Editing Cigarette (section)

==== Gateway theory ====
A very strong argument has been made about the association between adolescent exposure to nicotine by smoking conventional cigarettes and the subsequent onset of using other dependence-producing substances.{{sfn|SGUS|2016|p=106; Chapter 3}} Strong temporal and dose-dependent associations have been reported, and a plausible biological mechanism (via rodent and human modeling) suggests that long-term changes in the neural reward system take place as a result of adolescent smoking.{{sfn|SGUS|2016|p=106; Chapter 3}} Adolescent smokers of conventional cigarettes have disproportionately high rates of comorbid substance use, and longitudinal studies have suggested that early adolescent smoking may be a starting point or "[[Gateway drug theory|gateway]]" for substance use later in life, with this effect more likely for persons with [[attention deficit hyperactivity disorder]] (ADHD).{{sfn|SGUS|2016|p=106; Chapter 3}} Although factors such as genetic comorbidity, innate propensity for risk-taking, and social influences may underlie these findings, both human neuroimaging and animal studies suggest a neurobiological mechanism also plays a role.{{sfn|SGUS|2016|p=106; Chapter 3}} In addition, behavioral studies in adolescent and young adult smokers have revealed an increased propensity for risk-taking, both generally and in the presence of peers, and neuroimaging studies have shown altered frontal neural activation during a risk-taking task as compared with nonsmokers.{{sfn|SGUS|2016|p=106; Chapter 3}} In 2011, Rubinstein and colleagues used neuroimaging to show decreased brain response to a natural reinforcer (pleasurable food cues) in adolescent light smokers (1–5 cigarettes per day), with their results highlighting the possibility of neural alterations consistent with nicotine dependence and altered brain response to reward even in adolescent low-level smokers.{{sfn|SGUS|2016|p=106; Chapter 3}}