5.4 Adolescence and brain maturation

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 333¹) during adolescence.¹ Initiation of substance use during this time increases 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 people who smoke may rapidly become addicted, even at low levels of consumption,^2,4 and at significantly lower nicotine levels than adults.⁵ For example, preliminary research among young people aged 13–17 years found that light smoking (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 adults and teenagers who smoke heavily.⁵

Young people’s tobacco use and nicotine addiction have both been classified as paediatric medical disorders, rather than for example attributing tobacco consumption among young people 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.^7-9 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

Researchers have proposed 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

Research examining responsiveness to visual smoking cues has found adolescents who smoke to be more sensitive to visual cues depicting cigarette smoking behaviour than adults. This is thought to be due to ongoing ontogenetic changes in the brain which take place during adolescence, rendering adolescents susceptible to smoking cues and cravings due to heightened reward sensitivity and an underdeveloped ability to regulate cravings.¹⁵ Regions in the frontostriatal circuitry, including the ventral striatum and dorsolateral prefrontal cortex have been shown to be sensitive to cigarette cue reactivity. During adolescence the ventral striatum becomes hypersensitive to reward stimuli, and the dorsolateral prefrontal cortex, while still developing, cannot effectively regulate the adolescent’s cravings. Resulting in adolescents being more sensitive to visual smoking cues than adults.¹⁵

A 2022 systematic review on brain morphology predictors of tobacco and other substance use found that smaller amygdala volumes in adolescents was related to future daily tobacco smoking.¹⁶ However, it was only one study¹⁷ in the systematic review that related specifically to tobacco use; a 2018 prospective study conducted in Melbourne, Australia. The study investigated whether the volume of the amygdala and orbitofrontal cortex (OFC) mediate the relationship between externalising symptoms and daily smoking in adolescence. The findings revealed that smaller right amygdala volumes and externalising behaviours were significant predictors of daily smoking at age 18. Additionally, right amygdala volumes were found to mediate the relationship between externalising symptoms and later smoking, highlighting the importance of neurobiological factors in the development of substance use disorders and related psychopathology.¹⁷

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’.¹⁸ It is also likely that the social context in which early experimentation occurs will influence an individual’s perception of the experience.¹⁸ 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 13.

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.¹⁹ 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.²⁰ 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.²¹ 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;²² 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.²³ 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.²³ 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.²³

In addition, findings from a longitudinal Canadian study (following more than 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.²⁴

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.²⁵ 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 parental²⁰ and school connectedness, also mediate the effects of puberty.^19,26

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References

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