Nicotine Chemistry, Pharmacology, and Pharmacokinetics

McKinney, Diana L.; Vansickel, Andrea R.

doi:10.1016/b978-0-12-800213-1.00009-2

Cited by 7 publications

(8 citation statements)

References 55 publications

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“…On the other hand, moist snuff, snus, consist of fire and air-cured dark tobacco, while dry snuff comprises fermented and fire cured powder (Kindvall et al 2019 ; Pillitteri et al 2020 ). Apparently, the main motivating factor for an individual to use tobacco products is nicotine—a tobacco alkaloid constituting nearly 95% of tobacco chemicals (Ji et al 2017 ; McKinney and Vansickel 2016 ). When tobacco enters the human biological system in the form of smoke, numerous compounds constituting tobacco smoke are taken in by the smoker (Tsai et al 2018 ), which are initiators for generative and degenerative diseases including cancer and grave respiratory diseases, such as emphysema, asthma, cardio obstructive pulmonary disorder (COPD) (Ferrante and Conti 2017 ).…”

Section: Resultsmentioning

confidence: 99%

A review of tobacco abuse and its epidemiological consequences

Omare

Kibet

Cherutoi

et al. 2021

J Public Health (Berl.)

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Section: Resultsmentioning

confidence: 99%

A review of tobacco abuse and its epidemiological consequences

Omare

Kibet

Cherutoi

et al. 2021

J Public Health (Berl.)

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“…Variants within the CHRNA5-A3-B4 gene cluster which encodes for subunits of nAChR are among the most robust associations with nicotine dependence (42, 71-73) and have also been implicated in schizophrenia (53). Presynaptic activation of nAChR stimulates the release of several neurotransmitters including dopamine, serotonin and glutamate (74-77). Dysregulation of dopaminergic and glutamatergic pathways could both explain why some people may be more susceptible to the positive reinforcing effects of smoking (78) and have an increased vulnerability to develop schizophrenia (79).…”

Section: Discussionmentioning

confidence: 99%

Genetic overlap and causal associations between smoking behaviours and psychiatric traits and disorders in adolescents and adults

Barkhuizen

Dudbridge

Ronald

2020

Preprint

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Background: Epidemiological research shows that smoking is associated with psychiatric disorders and psychotic experiences, even after controlling for confounds such as cannabis use and sleep problems. We investigated degree of genetic overlap and tested for causal associations between smoking and psychiatric traits and disorders using genetic data. We tested whether genetic associations existed beyond genetic influences shared with confounding variables.Methods: Genetic correlations were estimated with LD-score regression between smoking behaviours (N=262,990-632,802) and psychiatric disorders (schizophrenia, bipolar disorder and depression; N=41,653-173,005), psychotic experiences in adolescents (N=6,297-10,098) and adults (N=116,787-117,794) and adult schizotypy (N=3,967-4,057). Genomic Structural Equation Modelling was performed to explore the associations while accounting for genetic influences of confounders (cannabis and alcohol use, risk-taking and insomnia). Causal associations were tested using Generalized Summary-based Mendelian Randomization (GSMR).Results: Significant genetic correlations were found between smoking and psychiatric disorders (rg = .10 -.38) and adult PE (rg = .33 -.40). After accounting for covarying genetic influences, genetic associations between most smoking phenotypes and schizophrenia and depression remained but not between smoking behaviours and bipolar disorder or most psychotic experiences. GSMR results supported a causal role of smoking initiation on psychiatric disorders and adolescent cognitive and negative psychotic experiences. Conclusions: Pleiotropy between smoking behaviours and schizophrenia and depressionexists beyond the common genetic basis of known confounders. Smoking also appears to be causally associated with psychiatric disorders and with cognitive PEs and negative symptoms during adolescence. Exploration of the biological links underlying smoking and psychiatric illness would be well-justified.

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“…The vascular endothelial dysfunction is associated with nicotine exposure, ROS, oxidative stress-driven inflammation, and decreased activity of Na + /K + /2Cl − cotransporter in the blood-brain barrier (BBB) [ 25 ]. Nicotine pharmacokinetics is correlated with its physicochemical properties and route of administration, with a rapid oral, intestinal, respiratory, and skin absorption, as well as the physiological system [ 26 ], with increased bioavailability via smoking or e-cig [ 27 ], reaching in seconds the arterial circulation and brain [ 24 ]. Its primarily metabolism is taking place in liver, leading to a major metabolite, cotinine, involving CYP450 2A6, aldehyde oxidase, flavin-containing monooxygenase 3, and uridine diphosphate-glucuronosyltransferase enzymes.…”

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confidence: 99%

“…Particularly, β2 containing nAchR mediates the reinforcing effects of nicotine. It has been demonstrated that nicotine long term exposure is correlated with strong desensitization of β2-type nAchRs, with a key role in nicotine addiction [ 26 ]. The reinforcement of nicotine effects is attributed to dopamine (DA) and dopaminergic pathways, while various factors have been demonstrated to affect nicotine metabolism, pharmacokinetics, and pharmacodynamics, such as physiological characteristics (gender, age, and diet), smoking behaviour, race, genetic polymorphism, medication, and certain diseases.…”

mentioning

confidence: 99%