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      Update on Safety Profiles of Vitamins B1, B6, and B12: A Narrative Review

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          Abstract

          The neurotropic B vitamins B1 (thiamine), B6 (pyridoxine), and B12 (cobalamin) are essential for proper functioning of the nervous system. Deficiencies may induce neurological disorders like peripheral neuropathy (PN) and mainly occur in vulnerable populations (eg, elderly, diabetics, alcoholics). As epidemiologic cohort studies raised safety concerns about vitamin B6/B12 intake being potentially associated with increased risks of hip fracture (HF) and lung cancer (LC), we explored these aspects and performed comprehensive literature searches. However, we suggest not to neglect actual high-risk factors (eg, smoking in LC, higher age in HF) by focusing on individual nutrients, but to examine the complex interaction of numerous factors involved in disease development. Because it warrants continued consideration, we also provide an update on neurotoxicity associated with vitamin B6. We consider that neurological side effects due to vitamin B6 intake are rare and only occur with high daily doses and/or longer treatment duration. The benefit-risk ratio of high-dose treatment with neurotropic B vitamins in indications like PN is therefore considered advantageous, particularly if dosing recommendations are followed and serum levels monitored.

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          Clinical practice. Vitamin B12 deficiency.

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            The relationship between COPD and lung cancer

            Highlights • COPD is a risk factor for lung cancer beyond their shared aetiology. • Both are driven by oxidative stress. • Both are linked to cellular aging, senescence and telomere shortening. • Both have been linked to genetic predisposition. • Both show altered epigenetic regulation of gene expression.
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              Smoking, p53 mutation, and lung cancer.

              This issue marks the 50th anniversary of the release of the U.S. Surgeon General's Report on Smoking and Health. Perhaps no other singular event has done more to highlight the effects of smoking on the development of cancer. Tobacco exposure is the leading cause of cancers involving the oral cavity, conductive airways, and the lung. Owing to the many carcinogens in tobacco smoke, smoking-related malignancies have a high genome-wide burden of mutations, including in the gene encoding for p53. The p53 protein is the most frequently mutated tumor suppressor in cancer, responsible for a range of critical cellular functions that are compromised by the presence of a mutation. Herein, we review the epidemiologic connection between tobacco exposure and cancer, the molecular basis of p53 mutation in lung cancer, and the normal molecular and cellular roles of p53 that are abrogated during lung tumor development and progression as defined by in vitro and in vivo studies. We also consider the therapeutic potential of targeting mutant p53 in a clinical setting based upon the cellular role of mutant p53 and data from genetic murine models.
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                Author and article information

                Journal
                Ther Clin Risk Manag
                Ther Clin Risk Manag
                tcrm
                tcriskman
                Therapeutics and Clinical Risk Management
                Dove
                1176-6336
                1178-203X
                22 December 2020
                2020
                : 16
                : 1275-1288
                Affiliations
                [1 ]Center for Research in Genetics and Genomics (CIGGUR), GENIUROS Research Group, School of Medicine and Health Sciences, Universidad del Rosario , Bogotá, Colombia
                [2 ]Neuroscience Research Group (NEUROS), School of Medicine and Health Sciences, Universidad del Rosario , Bogotá, Colombia
                Author notes
                Correspondence: Carlos-Alberto Calderon-Ospina School of Medicine and Health Sciences, Universidad del Rosario , Carrera 24 No. 63C–69, Bogota, DC, ColombiaTel +571-2970200 Ext 3318Fax +571-2818583 Email carlos.calderon@urosario.edu.co
                [*]

                These authors contributed equally to this work

                Author information
                http://orcid.org/0000-0002-7305-8727
                http://orcid.org/0000-0001-8458-7862
                http://orcid.org/0000-0002-4961-974X
                Article
                274122
                10.2147/TCRM.S274122
                7764703
                33376337
                d23931cc-9c83-482f-ba76-b2422887fe90
                © 2020 Calderon-Ospina et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                : 27 July 2020
                : 04 September 2020
                Page count
                Figures: 1, Tables: 6, References: 90, Pages: 14
                Categories
                Review

                Medicine
                neurotropic b vitamins,safety,thiamine,pyridoxine,cobalamin,neurotoxicity,hip fracture,lung cancer
                Medicine
                neurotropic b vitamins, safety, thiamine, pyridoxine, cobalamin, neurotoxicity, hip fracture, lung cancer

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