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Cancer
Published in Gia Merlo, Kathy Berra, Lifestyle Nursing, 2023
Alcohol increases cancer risk through several mechanisms (IARC Working Group on the Evaluation of Carcinogenic Risk to Humans, 2012; World Cancer Research Fund/American Institute for Cancer Research, 2018). Alcohol is metabolized to acetaldehyde, which is carcinogenic in humans. In addition, alcohol metabolism increases oxidative stress, and alcohol can increase circulating levels of estrogen, an established risk factor for breast cancer. Further risk can come from alcohol’s ability to serve as a solvent, facilitating carcinogen penetration into cells, which is considered a primary explanation for the synergistic increase in risk of mouth and throat cancers for people exposed to both alcohol and tobacco.
Dietary guidelines and recommendations
Published in Geoffrey P. Webb, Nutrition, 2019
The link between alcohol and cancer is not a new one, and increased deaths from cancer, liver disease and trauma have long been accepted as responsible for the rising mortality at higher alcohol doses. The 1995 Sensible drinking report also accepted that there was almost certainly a causal and dose-dependent link between alcohol consumption and certain cancers. These authors concluded that heavy drinking of over 60 units/week caused a 3–15 fold increase in risk depending upon the site, and evidence of increased risk from over 35 units/week was said to be convincing. They also said that they could not exclude the possibility that at intakes below 18 units per week there might be some small increase in relative risk but that the number of cases attributed to low levels of alcohol would be very small as the types of cancer caused by alcohol were relatively uncommon.
Nutrition and the Risk of Common Forms of Cancer
Published in David Heber, Zhaoping Li, Primary Care Nutrition, 2017
Based on extensive research, there is a scientific consensus for a connection between alcohol consumption and several types of cancer (IARC Working Group on the Evaluation of Carcinogenic Risks to Humans 2010, 2012). The National Toxicology Program of the U.S. Department of Health and Human Services lists consumption of alcoholic beverages as a known human carcinogen. The research evidence indicates that both the amount of alcohol consumed and the number of years of regular alcohol consumption contribute to the risk of developing an alcohol-associated cancer. Based on data from 2009, an estimated 3.5% of all cancer deaths in the United States (about 19,500 deaths) were alcohol related (Nelson et al. 2013).
Dietary Intake as Determinant Nongenetic Factors to Colorectal Cancer Incidence and Staging Progression: A Study in South Sulawesi Population, Indonesia
Published in Nutrition and Cancer, 2021
Ika Nurlaila, Alam A. Hidayat, Arif Budiarto, Bharuno Mahesworo, Kartika Purwandari, Bens Pardamean
As opposed to the fruits and vegetable intake effects, we figured out in our dataset that those who defined themselves as seldom-eaters of meat had a lower probability of suffering from CRC by 28.95% than those from often-eaters which probability is measured at 71.05%. In contrast, in the case-cohort, about 79.78% of people in the group consumed meat more frequently or in larger quantities compared to the healthy donor (20.22%). In line with this trend, frequent-alcohol drinker was observed in 82.55% of CRC cohort while seldom-drinkers made up 17.05% of the total of CRC patients. A study conducted by the European Prospective Investigation into Cancer and Nutrition (EPIC) demonstrated that heavy alcohol use correlated with a higher death risk due to alcohol-related cancer (29,30).
Aldehyde dehydrogenase-2 as a therapeutic target
Published in Expert Opinion on Therapeutic Targets, 2019
Mitsuru Kimura, Akira Yokoyama, Susumu Higuchi
Strong evidence suggesting that ALDH2 polymorphism is associated with the risk of alcohol-related cancer is available. The strongest association of this type was found in squamous cell carcinomas of the upper aerodigestive tract comprising of the oral cavity, pharynx, larynx, and esophagus [28]. In a Japanese multisite case-control study, the odds ratio for detecting esophageal cancer in the inactive ALDH2 group (ALDH2*1/*2) compared to that of the active ALDH2 group (ALDH2*1/*1) was 10.0-fold among moderate drinkers (198–395 g ethanol/week) and 8.6 fold among heavy drinkers (≥ 396 g ethanol/week) [29,30]. A meta-analysis performed on 31 case-control studies, mostly from China and Japan, reported the same result and the odds ratio was found to be 1.21, 3.79 and 6.50 among non- or rare drinkers, light drinkers (1–350 g ethanol/week), and heavy drinkers (≥ 350 g ethanol/week), respectively [31]. Similarly, another meta-analysis study revealed that a significant association exists between ALDH2 polymorphism and cancer of the head and neck. The presence of inactive ALDH2 increases the risk of head and neck cancer 1.68-fold and 3.57-fold among moderate and heavy drinkers, respectively, compared to those with active ALDH2 [32]. The carcinogenic effect is brought about by the high acetaldehyde concentration in the tissues. The inefficient degradation of acetaldehyde by inactive ALDH2 results in the formation of acetaldehyde-DNA adducts, which cause tissue cancerization. Garaycoechea et al. reported the mechanism of acetaldehyde-derived DNA damage using hematopoietic stem cells; acetaldehyde causes the formation of DNA interstrand crosslinks despite Fanconi anemia pathway mediated by FANCD2 repairs the DNA modifications, which results in increased mutagenesis [33]. Heavy alcohol consumption is also known to be associated with liver cancer, breast cancer, and colorectal cancer. However, the effect of ALDH2 polymorphism on the risk of these cancers is unclear, because few association studies on this have been reported, and their results are mixed [34].