The concept of exposure when selecting comparison groups for determining individual susceptibility to addiction to cigarette smoking

Abstract

Smoking is a leading cause of preventable death. The effect of tobacco is even more contundent in people with mental illness and, in general, cigarette smoking addiction is influenced by genetic factors. The opioid system is involved in the mesolimbic reward system, which is of great importance in addictive behaviors, such as smoking and is influenced by genes such as the OPRM1 . The aim of this study was to evaluate if selecting a comparison group that include light smokers versus people that never smoked impacts the results of genetic association studies. In addition, to evaluate the genetic association in different groups of smokers by analyzing independent covariates such as mental illness and clinical dental data. All subjects were participants of the Dental Registry and DNA Repository project. Genotyping was carried out using TaqMan chemistry for two markers in OPRM1 (rs553202 and rs7755635). Logistic regression analyses were performed as implemented in PLINK. The established value for alpha was 5%, and the Hardy-Weinberg equilibrium was evaluated by the chi-square test with one degree of freedom for each marker. 1,897 patients were included, which were allocated to eight distinct groups, according to the frequency and quantity of cigarettes smoked and mental illness status. There was no significant association between the two markers in OPRM1 and smoking. When mental illness and dental clinical data (tooth loss, dental caries, and periodontitis) were used as covariates, there were associations between heavy smoking and OPRM1 , when non-smokers were used as comparison. We did not have diet or microbiome data to consider for these dental analyses and suggest that these kinds of data should be always incorporated in the future. Significant results were found only when the covariables mental illness and oral clinical data were added to the analysis.

Nicotine promotes development of bile duct ligationinduced liver fibrosis by increasing expression of nicotinic acetylcholine receptors in rats

“…If we convert the human dose of nicotine to a rat dose, we get approximately 10 mg/kg every other day [29]. Therefore, the doses we chose for low and high doses of nicotine (1 or 10 mg/kg) are equivalent to the concentration of nic-otine found in light smokers and heavy smokers, respectively [30]. Some previous studies on normal rats or using various animal models of liver disease emphasize that nicotine may aggravate the process of liver fibrosis [31][32][33].…”

IRF6 Genetic Variation and Maternal Smoking During Pregnancy in Cleft Lip/Palate

“…Not wanting to be judged, people will hide this information. To improve homogeneity, one can suggest that individuals tested should have been exposed to the same risk factor (11), therefore here we tested for association only children that had maternal cigarette smoking positive history. This approach was aimed at minimizing recall bias and at the same time it increases homogeneity.…”