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      The Alcohol Flushing Response: An Unrecognized Risk Factor for Esophageal Cancer from Alcohol Consumption

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          Abstract

          Philip Brooks and colleagues discuss evidence linking the alcohol flushing response (predominantly due to ALDH2 deficiency) with a much higher risk of esophageal cancer from alcohol consumption.

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          Estimating the population attributable risk for multiple risk factors using case-control data.

          P. Bruzzi, S Green, D Byar … (1985)
          A straightforward and unified approach is presented for the calculation of the population attributable risk per cent (etiologic fraction) in the general multivariate setting, with emphasis on using data from case-control studies. The summary attributable risk for multiple factors can be estimated, with or without adjustment for other (confounding) risk factors. The relation of this approach to procedures in the literature is discussed. Given values of the relative risks for various combinations of factors, all that is required is the distribution of these factors among the cases only. The required information can often be estimated solely from case-control data, and in some situations relative risk estimates from one population can be applied to calculation of attributable risk for another population. The authors emphasize the benefits to be obtained from logistic regression models, so that risks need not be estimated separately in a large number of strata, some of which may contain inadequate numbers of individuals. This approach allows incorporation of important interactions between factors, but does not require that all possible interactions be included. The approach is illustrated with data on four risk factors from a pair-matched case-control study of participants in a multicenter breast cancer screening project.
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            Overview of the role of alcohol dehydrogenase and aldehyde dehydrogenase and their variants in the genesis of alcohol-related pathology.

            Alvin Matsumoto, Min You, D Crabb … (2004)
            Alcohol dehydrogenase (ADH) and mitochondrial aldehyde dehydrogenase (ALDH2) are responsible for metabolizing the bulk of ethanol consumed as part of the diet and their activities contribute to the rate of ethanol elimination from the blood. They are expressed at highest levels in liver, but at lower levels in many tissues. This pathway probably evolved as a detoxification mechanism for environmental alcohols. However, with the consumption of large amounts of ethanol, the oxidation of ethanol can become a major energy source and, particularly in the liver, interferes with the metabolism of other nutrients. Polymorphic variants of the genes for these enzymes encode enzymes with altered kinetic properties. The pathophysiological effects of these variants may be mediated by accumulation of acetaldehyde; high-activity ADH variants are predicted to increase the rate of acetaldehyde generation, while the low-activity ALDH2 variant is associated with an inability to metabolize this compound. The effects of acetaldehyde may be expressed either in the cells generating it, or by delivery of acetaldehyde to various tissues by the bloodstream or even saliva. Inheritance of the high-activity ADH beta2, encoded by the ADH2*2 gene, and the inactive ALDH2*2 gene product have been conclusively associated with reduced risk of alcoholism. This association is influenced by gene-environment interactions, such as religion and national origin. The variants have also been studied for association with alcoholic liver disease, cancer, fetal alcohol syndrome, CVD, gout, asthma and clearance of xenobiotics. The strongest correlations found to date have been those between the ALDH2*2 allele and cancers of the oro-pharynx and oesophagus. It will be important to replicate other interesting associations between these variants and other cancers and heart disease, and to determine the biochemical mechanisms underlying the associations.
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              DNA adducts from acetaldehyde: implications for alcohol-related carcinogenesis.

              Jacob Theruvathu, Ralph Brooks (2005)
              Alcoholic beverage consumption is classified as a known human carcinogen, causally related to an increased risk of cancer of the upper gastrointestinal tract. The formation of acetaldehyde from ethanol metabolism seems to be the major mechanism underlying this effect. Acetaldehyde is carcinogenic in rodents and causes sister chromatid exchanges and chromosomal aberrations in human cells. The best-studied DNA adduct from acetaldehyde is N(2)-ethyl-2'-deoxyguanosine, which is increased in liver DNA obtained from ethanol-treated rodents and in white blood cells obtained from human alcohol abusers. However, the carcinogenic relevance of this adduct is unclear in view of the lack of evidence that it is mutagenic in mammalian cells. A different DNA adduct, 1,N(2)-propano-2'-deoxyguanosine (PdG), can also be formed from acetaldehyde in the presence of histones and other basic molecules. PdG has been shown to be responsible for the genotoxic and mutagenic effects of crotonaldehyde. The PdG adduct can exist in either of two forms: a ring-closed form or a ring-opened aldehyde form. Whereas the ring-closed form is mutagenic, the aldehyde form can participate in the formation of secondary lesions, including DNA-protein cross-links and DNA interstrand cross-links. The formation of these types of complex secondary DNA lesions resulting from PdG may explain many of the observed genotoxic effects of acetaldehyde described above. Repair of PdG and its associated adducts is complex, involving multiple pathways. Inherited variation in the genes encoding the proteins involved in the repair of PdG and its secondary adducts may contribute to susceptibility to alcoholic beverage-related carcinogenesis.
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                Author and article information

                Journal
                Journal ID (nlm-ta): PLoS Med
                Journal ID (publisher-id): pmed
                Journal ID (publisher-id): plme
                Journal ID (pmc): plosmed
                Title: PLoS Medicine
                Publisher: Public Library of Science (San Francisco, USA )
                ISSN (Print): 1549-1277
                ISSN (Electronic): 1549-1676
                Publication date (Print): March 2009
                Publication date (Electronic): 24 March 2009
                Volume: 6
                Issue: 3
                Electronic Location Identifier: e1000050
                Author notes
                * To whom correspondence should be addressed. E-mail: pjbrooks@ 123456mail.nih.gov ; a_yokoyama@ 123456kurihama1.hosp.go.jp
                Article
                Publisher ID: 08-PLME-RIT-3174R2
                DOI: 10.1371/journal.pmed.1000050
                PMC ID: 2659709
                PubMed ID: 19320537
                SO-VID: d1d250e8-aa18-4357-9b3c-1282b76bb2cb
                Copyright © This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration, which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.
                History
                Page count
                Pages: 6
                Categories
                Subject: Research in Translation
                Subject: Gastroenterology and Hepatology
                Subject: Genetics and Genomics
                Subject: Oncology
                Subject: Public Health and Epidemiology
                Custom metadata
                citation Brooks PJ, Enoch M-A, Goldman D, Li T-K, Yokoyama A (2009) The alcohol flushing response: An unrecognized risk factor for esophageal cancer from alcohol consumption. PLoS Med 6(3): e1000050. doi: 10.1371/journal.pmed.1000050

                ScienceOpen disciplines: Medicine
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                ScienceOpen disciplines: Medicine

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