5.4 Physiological aspects
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5.4.1 Genetics
Greater understanding of human genetics has led to enquiry into whether genetic make-up affects an individual's likelihood of smoking. Data from family, adoption and most especially twins studies has shown that genetic make-up may contribute to the likelihood of smoking.16-19 Twin studies have variously reported that heritability for smoking (that is to say, the proportion in the variance in smoking that is attributable to genetic factors) ranges from about 50%–80%, which is in keeping with heritability estimates for alcoholism, asthma, and hypertension.18 Inherited factors influencing initiation and dependence are likely to overlap, to some degree, but there is evidence that independent genetic influences may mediate each stage of tobacco use.20-22 For example, one review of the data has estimated that in twins, about 60% of the liability to initiate smoking can be attributed to genetic influences.16 Genetic predisposition to tobacco use may, however, be modified by other individual and environmental factors, such as family structure, religion and marital status.17
Smoking is understood to be a highly complex behaviour, and where a genetic basis may be postulated, it is with the recognition that many genes are likely to be involved, each contributing only a small degree of influence singly. Candidate genes for investigation in tobacco initiation, dependence and persistence have included several known to affect neurotransmitter pathways, nicotine-specific pathways, and nicotine metabolism. Other genes connected with traits such as depression and anxiety are also being studied.17 There is also emerging evidence that genetic factors may influence an individual's choice of friends, and that some individual's genetic make-up may make them more susceptible to the influence of peer groups.23
The role of genes in smoking behaviour is discussed further in Chapter 6, Section 6.4.
5.4.2 Effect of maternal smoking in utero on uptake of smoking in offspring
Several studies from Australia24, 25 and internationally have reported an association between smoking during pregnancy and subsequent increased likelihood of uptake of smoking in offspring, even after controlling for a range of confounding factors.26-30 It may be that effects are different depending on the sex of the baby, some research suggesting that female offspring are more susceptible to later uptake of smoking than males.30 However other research suggests that the effects of maternal smoking may not persist beyond early adolescence, after which social factors (such as mother's current smoking behaviour and peer smoking) appear to become more important.31
There is a plausible physiological connection between maternal smoking and in utero effects on the brain. It is known that nicotine present in tobacco smoke reaches the unborn child through the placenta, binding with and activating neurotransmitters in the central and peripheral nervous system and negatively affecting neurodevelopment. However the exact mechanisms and long-term consequences of these effects has not been fully elucidated.32
5.4.3 Adolescence and brain maturation
The human brain does not reach full maturation until late adolescence or early adulthood, with significant changes to brain structure occurring during adolescence. Research suggests that adolescence marks a period of heightened biological sensitivity to the stimulatory and reinforcing properties of nicotine.33 Young smokers may rapidly become addicted to smoking, even at low levels of consumption,34 a factor likely to be mediated by comparative brain immaturity.4, 35, 36 Adolescent exposure to nicotine may trigger long-term changes in brain function relating to reward pathways, learning, memory and mood37 as well as a permanent susceptibility to nicotine addiction.38 These changes may also predispose the individual to later use of other addictive substances, and to mental illness.39
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'.7 However it is also likely that the social context in which early experimentation occurs will influence an individual's perception of the experience.7 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 6.7.
5.4.4 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.40 Recent research from the USA has shown that early maturers are twice as likely to try cigarettes as adolescents with an average age of physical maturity.41
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.42 The increase in sensation seeking and risk-taking associated with puberty, may come into play before other parts of the brain responsible for weighing consequences and exert judgement reach maturity.39 However social context, such as peer group smoking behaviours and attitudes, and parental41 and school connectedness, also mediate the effects of puberty.40
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