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      Electronic Cigarette Harms: Aggregate Evidence Shows Damage to Biological Systems

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          Abstract

          Evidence of the harms of e-cigarettes has been unfolding slowly and has been documented in many reviews and reports worldwide. A narrative review of new evidence is presented since, as research has continued, newly aggregated evidence of the dangers of electronic cigarettes on the brain, heart, and lungs is vital to inform decisions on restricting the use of e-cigarettes. Several biomedical research databases were searched for electronic cigarette health effects, emphasizing reviews, systematic reviews, and meta-analyses. Over 50 review studies, primarily in 2022 and 2023, illustrate some of the latest information on e-cigarette harms. Results show studies of respiratory, neurological, and cardiovascular effects. Researchers call for expanding studies through new methods to elaborate on initial findings of multiple harms emerging in clinical investigations. Since the use of electronic cigarettes for adult cessation is not sanctioned in most countries, it is clear that health authorities see significant costs to the health of the general population if the promotion and use of electronic cigarettes occur worldwide. Regulatory action to control electronic cigarettes should consider the substantial evidence of electronic cigarette harm.

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          Probability and predictors of transition from first use to dependence on nicotine, alcohol, cannabis, and cocaine: results of the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC).

          This study aims to estimate general and racial-ethnic specific cumulative probability of developing dependence among nicotine, alcohol, cannabis or cocaine users, and to identify predictors of transition to substance dependence. Analyses were done for the subsample of lifetime nicotine (n=15,918), alcohol (n=28,907), cannabis (n=7389) or cocaine (n=2259) users who participated in the first and second wave of the National Epidemiological Survey on Alcohol and Related Conditions (NESARC). Discrete-time survival analyses were implemented to estimate the cumulative probability of transitioning from use to dependence and to identify predictors of transition to dependence. The cumulative probability estimate of transition to dependence was 67.5% for nicotine users, 22.7% for alcohol users, 20.9% for cocaine users, and 8.9% for cannabis users. Half of the cases of dependence on nicotine, alcohol, cannabis and cocaine were observed approximately 27, 13, 5 and 4 years after use onset, respectively. Significant racial-ethnic differences were observed in the probability of transition to dependence across the four substances. Several predictors of dependence were common across the four substances assessed. Transition from use to dependence was highest for nicotine users, followed by cocaine, alcohol and cannabis users. Transition to cannabis or cocaine dependence occurred faster than transition to nicotine or alcohol dependence. The existence of common predictors of transition dependence across substances suggests that shared mechanisms are involved. The increased risk of transition to dependence among individuals from minorities or those with psychiatric or dependence comorbidity highlights the importance of promoting outreach and treatment of these populations. Published by Elsevier Ireland Ltd.
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            Nicotine Gateway Effects on Adolescent Substance Use

            Given the rise in teenage use of electronic nicotine delivery systems (“vaping”) in congruence with the increasing numbers of drug-related emergencies, it is critical to expand the knowledge of the physical and behavioral risks associated with developmental nicotine exposure. A further understanding of the molecular and neurochemical underpinnings of nicotine’s gateway effects allows emergency clinicians to advise patients and families and adjust treatment accordingly, which may minimize the use of tobacco, nicotine, and future substances. Currently, the growing use of tobacco products and electronic cigarettes among teenagers represents a major public health concern. Adolescent exposure to tobacco or nicotine can lead to subsequent abuse of nicotine and other substances, which is known as the gateway hypothesis. Adolescence is a developmentally sensitive time period when risk-taking behaviors, such as sensation seeking and drug experimentation, often begin. These hallmark behaviors of adolescence are largely due to maturational changes in the brain. The developing brain is particularly vulnerable to the harmful effects of drugs of abuse, including tobacco and nicotine products, which activate nicotinic acetylcholine receptors (nAChRs). Disruption of nAChR development with early nicotine use may influence the function and pharmacology of the receptor subunits and alter the release of reward-related neurotransmitters, including acetylcholine, dopamine, GABA, serotonin, and glutamate. In this review, we emphasize that the effects of nicotine are highly dependent on timing of exposure, with a dynamic interaction of nAChRs with dopaminergic, endocannabinoid, and opioidergic systems to enhance general drug reward and reinforcement. We analyzed available literature regarding adolescent substance use and nicotine’s impact on the developing brain and behavior using the electronic databases of PubMed and Google Scholar for articles published in English between January 1968 and November 2018. We present a large collection of clinical and preclinical evidence that adolescent nicotine exposure influences long-term molecular, biochemical, and functional changes in the brain that encourage subsequent drug abuse.
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              Brain lesions disrupting addiction map to a common human brain circuit

              Drug addiction is a public health crisis for which new treatments are urgently needed. In rare cases, regional brain damage can lead to addiction remission. These cases may be used to identify therapeutic targets for neuromodulation. We analyzed two cohorts of patients addicted to smoking at the time of focal brain damage (cohort 1 n = 67; cohort 2 n = 62). Lesion locations were mapped to a brain atlas and the brain network functionally connected to each lesion location was computed using human connectome data (n = 1,000). Associations with addiction remission were identified. Generalizability was assessed using an independent cohort of patients with focal brain damage and alcohol addiction risk scores (n = 186). Specificity was assessed through comparison to 37 other neuropsychological variables. Lesions disrupting smoking addiction occurred in many different brain locations but were characterized by a specific pattern of brain connectivity. This pattern involved positive connectivity to the dorsal cingulate, lateral prefrontal cortex, and insula and negative connectivity to the medial prefrontal and temporal cortex. This circuit was reproducible across independent lesion cohorts, associated with reduced alcohol addiction risk, and specific to addiction metrics. Hubs that best matched the connectivity profile for addiction remission were the paracingulate gyrus, left frontal operculum, and medial fronto-polar cortex. We conclude that brain lesions disrupting addiction map to a specific human brain circuit and that hubs in this circuit provide testable targets for therapeutic neuromodulation.
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                Author and article information

                Journal
                IJERGQ
                International Journal of Environmental Research and Public Health
                IJERPH
                MDPI AG
                1660-4601
                October 2023
                September 22 2023
                : 20
                : 19
                : 6808
                Article
                10.3390/ijerph20196808
                10572885
                37835078
                ddd08412-72c6-4aa6-97ce-c62f4c5dc1bf
                © 2023

                https://creativecommons.org/licenses/by/4.0/

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