This study investigated two separate questions about the relationship between PE and tobacco use. First, we established that associations between tobacco use and specific types of PE were present during adolescence and remained for most PE after controlling for several covariates. Second, this was the first twin study to investigate the degree to which genetic and environmental influences explain the association between tobacco use and PE. Tobacco use was associated with paranoia and cognitive disorganization largely due to overlapping genetic influences, and with hallucinations due to familial influences that may include genes and shared environment.

Our results suggest that some of the same genetic factors that influence tobacco use in adolescents also influence PE. These results may also indicate gene−environment correlations whereby the genetic factors that influence PE create environments that make tobacco use more likely, and vice versa. Although the genetic correlation could indicate a causal association between PE and tobacco use in either direction, this was beyond the scope of this paper.

Our finding that tobacco use is associated with PE in adolescents is in line with previous findings. Gage et al.⁵ found an association between tobacco at age 16 years and PE at age 18 after controlling for cannabis use, familial depression, maternal education, IQ, bullying, and childhood psychosocial issues. McGrath et al.⁶ reported that those who commenced smoking before the age of 15 years were more likely to experience hallucinations at age 21. We found similar evidence while accounting for confounders not previously considered, such as sleep disturbance and SLE.

Tobacco use predicted PE to a lesser extent after including covariates, and adjusted models explained more variation in PE than models for tobacco use only. Therefore, some of the association between tobacco use and PE was attributable to the covariates tested, most notably to sleep disturbance. Considering these results and the known etiological association between PE and sleep disturbance,²⁴ future studies could explore the relationship between PE, tobacco use, and sleep disturbance. A previous TEDS study concluded that PE and cannabis use co-occurred due to shared environmental factors.²¹ In our analyses, we controlled for confounding by several other (environmental) factors, which may explain why cannabis use did not predict PE here.

We found regular smoking to be associated with paranoia, hallucinations, cognitive disorganization, and parent-rated negative symptoms, the latter two being less commonly studied compared to positive PE. The relationship between tobacco use and anhedonia diverged from this trend. Occasional smoking appears to be associated with lower anhedonia, but regular smoking, albeit not significantly, with higher anhedonia. Perhaps adolescents who experimented with tobacco, but not those who habitually smoked, were more likely to engage in pleasure-seeking behavior. Negative symptoms were parent-rated, whereas anhedonia was self-rated, which may partly account for different effect sizes between these PE types.

Another finding was that 50% of variation in adolescent tobacco use was due to common environmental influences and a third due to additive genetics. Twin studies have previously investigated the heritability of adolescent smoking.³⁰ Estimates of heritability and environmental influences can change over time and are context and population specific.³⁹ Anti-smoking regulations, legislation, and social attitudes toward smoking have changed rapidly over recent years. Between the early 2000s and the current study, the United Kingdom has banned smoking in public places, increased the legal age for purchasing tobacco products, introduced bold health warnings on tobacco products, restricted advertising, increased prices, and made nicotine replacement therapies more accessible.⁴⁰

A consideration is our operationalization of the tobacco use variable. We chose a three-level rather than a binary definition to improve power and to distinguish between the effects of regular and occasional smoking, in line with previous studies.2, 5 Our twin models assume linearity among not smoking, occasional smoking, and regular smoking. The prior regression analyses showed a linear association between tobacco use with paranoia, hallucinations, and cognitive disorganization, which supports this assumption. We note that anhedonia showed a nonlinear pattern, which could be explored in future research.

Our study was not designed to assess nicotine dependency, as never-smokers, for whom susceptibility to dependency is unknown, were included in our tobacco use measure. It is known that there may be some etiological differences between smoking initiation and nicotine dependency.⁴¹ We also cannot rule out attrition bias, because participating families were more likely to report higher socio-economic status than nonparticipating families.

The association between PE and tobacco use is significant and modest, and findings should be viewed in this context. We could not distinguish between genetic and common environmental influences shared between tobacco use and hallucinations, likely because the phenotypic correlation was lower than for our other bivariate models. Low phenotypic correlations also meant that we could not perform bivariate models between tobacco with grandiosity, anhedonia, and parent-rated negative symptoms.

Adolescent tobacco use is modifiable risk factor. Understanding the nature of the association between PE, a possible early manifestation of psychiatric disorder in some individuals, and tobacco use is of great interest. We have contributed to this field by showing that significant associations exist between specific PE domains and tobacco use in mid-adolescence that are not fully accounted for by confounding factors. We have provided novel insights into the etiology of the covariation between some PE and tobacco use that may inform further molecular genetic studies and developmental models.