The relationship between psychotic experiences and regular smoking during adolescence: A genetically sensitive design

BACKGROUND  High rates of smoking among individuals with psychiatric disorders is well documented. Few studies have investigated an association between smoking tobacco and psychotic experiences (PEs) in non-clinical samples.... [ view full abstract ]

BACKGROUND 

High rates of smoking among individuals with psychiatric disorders is well documented. Few studies have investigated an association between smoking tobacco and psychotic experiences (PEs) in non-clinical samples. Of those that have, none considered the full spectrum of PEs while controlling for cannabis use. This study aimed to investigate whether tobacco predicts specific PEs over and above cannabis use, and to estimate the genetic and environmental contributions to regular smoking in healthy adolescents.

METHODS

The Specific Psychotic Experiences Questionnaires was used to assess 3,787 twin pairs from the Twins Early Development Study. Twins reported on substance use and PEs including paranoia, hallucinations, grandiosity, cognitive disorganisation and anhedonia. Parents reported on the twins’ negative symptoms. Multiple linear regression models were conducted to control for cannabis use. Univariate liability threshold structural equation model-fitting was conducted on regular versus non-regular smokers to estimate the contributions of additive genetic (A), shared environmental (C) and unique environmental (E) influences. 

RESULTS

Tobacco and cannabis use both significantly predicted paranoia (β=17.40, t(3527)=4.13, p<.001), hallucinations (β=7.22, t(3531)=2.98, p=.003) and cognitive disorganisation (β=4.40, t(3530)=4.01, p<.001). In contrast, only tobacco, and not cannabis, predicted negative symptoms (β=5.78, t(3507)=3.80, p<.001) and anhedonia (β=19.84, t(3528)=6.49, p<.001). Twin modelling indicated an ACE model provided the best fit (BIC= -36824.12; AIC= -8168.68), with estimates of A, C, and E of 37%, 54% and 9%, respectively.

CONCLUSIONS

These findings cast further light on the relationship between tobacco and PEs, indicating that tobacco is associated with a range of non-clinical PEs. These results have implications for developmental theories on the role of substance use in early risk for psychiatric disorders. Further analyses should explore the degree to which phenotypic causality, and overlapping genetic and environmental influences, can explain the association between specific PEs and regular smoking.