this review summarizes the peer-reviewed literature on the neurocognitive and neurobiological implications of chronic cigarette smoking in cohorts that were not seeking treatment for substance use or psychiatric disorders. for reviews on the effects of chronic smoking on brain neurobiology and function in alcohol and substance use disorders see [13–15]. some studies observed the performance of former smokers fell between that of current smokers and nsc in young , middle-aged and older adults [31,35,39]. however, there are a few of computed tomography (ct) and magnetic resonance (mr)-based studies that suggest the reported neurocognitive deficiencies in smokers may be, in part, mediated by abnormalities in brain morphology, perfusion and/or neurochemistry. when investigating chronic cigarette smoking-induced neurobiological and neurocognitive dysfunction alone, or in conjunction with aud and other conditions, it is important to distinguish the effects of acute nicotine ingestion and withdrawal from the potential consequences of chronic exposure to the multitude of noxious compounds contained in cigarette smoke.
there are several potential mechanisms that may contribute independently, or in concert, to the neurobiological and neurocognitive abnormalities in chronic smokers. however, a significant amount of data regarding potential mechanisms contributing to the neurobiological and neurocognitive abnormalities observed in humans is derived from in vitro and animal studies. the vast majority of studies investigating the neurocognitive consequences of chronic cigarette smoking have been conducted in middle aged and older adults. the vast majority of studies assessing the neurocognitive and neurobiological consequences of chronic smoking are cross-sectional in design. such longitudinal studies are required to inform the development of more effective pharmacological and behavioral interventions to reduce the ever-increasing worldwide mortality and morbidity associated with the modifiable health risk that is chronic cigarette smoking.
tobacco use is a chronic relapsing disease, and remains the leading cause of preventable death in much of the world. the aim of this commentary is to try to reconcile this paradox, and offer an alternative approach to modeling changes in tobacco use status. a peculiar feature of the medical assessment of tobacco use is that it differs markedly from the assessment of other chronic diseases. but labeling someone an ex-smoker, whether by self-report or a negative response to recent use of tobacco products, imputes a durability to the state of “ex-smokerness” that may not last. carbon monoxide (co) is a product of tobacco combustion, and is commonly found in the exhaled breath of smokers.
the primary barrier to more widespread use of anabasine is the cost of the assay; in addition, it is not easily available in clinical laboratories. in addition, to the extent that there is no safe level of tobacco use, dichotomizing tobacco-relevant biomarkers to indicate use or non-use is clinically sensible. in making this important change, we will reinforce, among clinicians, health systems, and patients, that tobacco use is a recurring and remitting behavior, simplify the collection of clinically pertinent assessments of use, quit the focus on quitting, and shift our attention to ongoing treatment. a new clinical taxonomy for rating change in functional activities of patients with angina pectoris. anabasine and anatabine as biomarkers for tobacco use during nicotine replacement therapy. bat contributed to the intellectual content and writing of the manuscript.
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