5.3.1 Genetics
Greater understanding of the human genome has led to enquiry into whether genetics can affect an individual's chances of becoming an established smoker. Data from family, adoption and in particular twin studies have suggested that genetic makeup could contribute to the likelihood of both experimentation and progression to established patterns of smoking.1–5 In 2010, the US Surgeon General reported that 'genes appear to predispose persons to smoking initiation and persistence and possibly are related to the extent of difficulty a person has in smoking cessation'.6(page 156) 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 around 50–80%, which is in keeping with heritability estimates for alcoholism, asthma and hypertension.3
While inherited factors influencing initiation and dependence are likely to overlap to some degree, there is evidence that independent genetic influences may mediate each stage of tobacco use.2 ,7–9 For example, one review of the data has estimated that, in twins, around 60% of the liability to initiate smoking can be attributed to genetic influences.1 However, environmental influences10 also play an important role in nicotine dependence and frequency of smoking,6, 11 and genetic predisposition to tobacco use may be modified by individual and environmental factors such as family structure, religion and marital status.2
Interactions between genetic and environmental influence, and the causes of the relationships between social risk factors and substance use, may change significantly over the course of development. For example, evidence from twin research found that as twins developed from childhood to adulthood, the influence of shared environmental factors on church attendance (a consistent predictor of nicotine and alcohol consumption) declined dramatically, while the role of genetic factors increased.5 Frequent church attendance in adolescence appeared to reflect a range of shared familial and social–environmental influences that were protective against substance use, while in adulthood the inverse relationship between church attendance and substance use became stronger, stemming largely from genetically influenced temperamental factors.5
Genetic influences may mediate the association between social factors (such as adolescents' peer characteristics, including peer smoking) and smoking behaviour (including nicotine dependence) in other ways;10, 12 for example, adolescents with specific genetic risk for nicotine dependence may be less affected by social context such as peer smoking than those with lower risk genotypes.12 The evidence regarding potential gender differences in the relative importance of genetic and shared environmental influences for adolescent smoking behaviour and nicotine dependence is mixed,6, 13 while the extent of interaction between environmental and genetic risk factors in increasing susceptibility to nicotine addiction is unknown.14
Smoking is understood to be a highly complex behaviour, and where a genetic basis is postulated, it is with the recognition that many genes are likely to be involved, each individually contributing only a small degree of influence. Candidate genes for investigation in tobacco initiation, dependence and persistence have included several known to affect neurotransmitter pathways, nicotine-specific pathways and nicotine metabolism.2 The inheritance of genetic material may include polymorphisms of such genes, affecting individuals' physiological responses to nicotine, such as the rate of nicotine metabolism, receptor sensitivity to nicotine and to certain neurotransmitters, and the levels of neurotransmitters available at neural synapses. These individual differences in response to nicotine are likely to affect the trajectory toward the development of nicotine dependence.6 Other genes connected with traits such as depression and anxiety are also being studied.2 There is also emerging evidence that genetic factors may influence an individual's choice of friends, and that some individuals' genetic makeup may make them more susceptible to the influence of peer groups.15
Baler and Volkow13 describe the power of genetic variations, even at the level of a single gene, to affect performance in key behavioural circuits and subsequently impact on addiction risk. Behavioural circuits are being developed constantly due to interaction between genes and experience, resulting in the formation of attitudes, temperaments and, often, fixed behavioural patterns. During this maturation there are numerous opportunities to introduce risk or resilience into the system, as so many complex and overlapping developmental processes are taking place; this will influence subsequent individual tendencies such as those towards risk taking, for example.13
The role of genes in smoking behaviour is discussed further in Chapter 6, Section 4.
5.3.2 Effect of maternal smoking in utero on uptake of smoking in offspring
Several studies from Australia16,17 and internationally18–22 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. It may be that effects are different depending on the sex of the baby, with some research suggesting that female offspring exposed to tobacco smoke prenatally are more susceptible to taking up smoking as adolescents than male offspring similarly exposed.22
The relationship between maternal smoking and subsequent smoking uptake by offspring might be partially explained by their shared genetic background.6 Mothers who continue to smoke after pregnancy may also affect children's attitude to smoking through role modelling.6 Findings of at least one study suggest 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.23
However a connection between maternal smoking and in utero effects on the brain is physiologically plausible. While the exact mechanisms and long-term consequences of these effects have not been fully elucidated24 it is known that nicotine (a toxic chemical) 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. Chronic exposure to nicotine during prenatal development has been shown in some animal studies to affect reward-related neural circuitry, in turn modifying the psychoactive effects of drugs in later life.25 A behavioural study among Canadian adolescents found that participants who had been prenatally exposed to maternal tobacco smoke were significantly more likely to use an addictive substance later in life, even after controlling for other variables such as age and peer drug use.25 Investigators suggested that prenatal exposure to maternal smoking could interfere with cortical development (important in decision-making) via modification of the gene that produced 'brain-derived neurotrophic factor' (BDNF); this in turn could influence adolescent susceptibility to addiction through abnormal processing of reward-associated cues, facilitating impulsive behaviours and subsequently higher substance abuse rates.13, 25
5.3.3 Exposure to secondhand smoke
While exposure to secondhand smoke (SHS) has long been known to cause serious diseases6, it has also been associated with increased risk for initiation26, maintenance of cigarette smoking26-29 and intention to smoke in the future.26 Indoor and enclosed environments are of particular concern. SHS exposure in the home or car is associated with smoking initiation a young age.26 It is possible that exposure to SHS can stimulate neural pathways which increase the brains sensitivity to nicotine prior to active smoking.26
Non-smokers exposed to high levels of SHS may absorb amounts of nicotine similar to smokers.29 For example, research examining the effects of SHS exposure on nicotinic acetylcholine receptors in the brain found that both smoking and non-smoking participants who were exposed to SHS for one hour as car passengers experienced significant receptor occupancy and increased plasma nicotine concentrations.27
An exploratory US study investigated whether sensitivity to SHS exposure (assessed with reaction measures commonly used to gauge subjective reactivity to the first experience with smoking cigarettes) among never-smokers aged 8–13 years predicted susceptibility to smoking (measured through likelihood of future smoking).28 Those who reported more negative experiences with SHS exposure (such as coughing or feeling sick) tended to be less susceptible to smoking than those who experienced fewer unpleasant reactions. Some evidence was found for decreasing sensitivity to SHS with age.28 Children are especially susceptible to the effects of nicotine exposure through SHS, in part due to the differing effects of nicotine pharmacokinetics between children and adults.29
Exposure to smoke in social situations (quantified as the number of current smokers in the social environment and number of situations where SHS exposure occurs), has been found to predict precursors to smoking initiation (including perceived nicotine dependence and smoking susceptibility) among adolescent never-smokers.29 A large 2011 US survey involving students aged 12–17 years found exposure to secondhand smoke (as measured by frequency of exposure during the previous week and smoking in the home) was as influential in prompting uptake of smoking as peer pressure and exposure to tobacco advertising.30
In addition to a shared genetic predisposition to smoke and role modelling of smoking behaviour,29 cumulative exposure to secondhand smoke may increase risk for smoking uptake through additional exposure to nicotine during a time of critical brain development.28
5.3.4 Childhood illness and smoking uptake
The occurrence of asthma during childhood may be associated with reduced smoking uptake among male adolescents, but not females.31 Quality of life (QOL) and smoking have been shown to be related in studies among healthy and illness populations.32 The assumption that smoking causes a reduction in QOL was supported in some longitudinal studies, while other longitudinal research found that changes in smoking status did not predict QOL changes.32
A longitudinal study investigating whether the outcomes of asthma predicted smoking onset among adolescents with asthma found that poorer self-reported medication adherence and the maladaptive coping strategy of hiding asthma predicted smoking onset among both girls and boys, while poorer QOL predicted smoking in boys only.32 There is some evidence of an indirect relationship between asthma and smoking behaviour from a prospective population-based study conducted among Dutch adolescents. Participants with current asthma were more likely to report depressive feelings (as opposed to depression or depressive symptoms) than those without asthma: specifically, those with current, severe symptoms of asthma were more likely to report depressive feelings than respondents with mild and moderate symptoms. However, smoking behaviour was similar for adolescents with and without asthma. Depressive feelings and smoking were related both cross-sectionally and longitudinally.33
A systematic review investigating tobacco use among adolescents with physical disabilities found that those with physical disabilities were significantly more likely to use tobacco, compared to adolescents without physical disabilities.34 Similar to adolescents with severe asthma being more likely to report depressive feelings, adolescents with physical disabilities may also experience greater stressors and discrimination, which is associated with negative health behaviours such as tobacco use.34
There is a strong relationship between adolescent smoking and a range of psychiatric conditions; these are discussed further in Section 5.5.2 and Section 9A.3.
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References
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