However, some of the associations among alcohol drinking premenopausal women were limited to those taking oral contraceptives [40]. Many observational studies have been conducted to identify and define the risks from drinking alcohol and cancer development. Some limitations in these studies have been identified, vanderburgh house such as lack of sufficient adjustment of confounding factors, for example tobacco smoking and alcohol consumption are both common risk factors for oral cavity cancer. There are also concerns around reverse causality, with the reference categories of alcohol non-drinkers possibly including former drinkers who still have an elevated risk of cancer. There are other concerns over the accuracy of recording of alcohol exposure data where bias may be incorporated through non-participation of heavy drinkers in health studies, and under-reporting of alcohol consumption by the study subjects.
All of the water- drinking animals had developed visible lung metastases at 16 days after tumor injection, whereas some of the ethanol-drinking mice did not develop lung metastases until 21 days. More-over, the numbers of lung metastases in the ethanol-drinking mice were significantly lower at 21 days. Other researchers investigated the effects of alcohol on metastasis of the estrogen receptor–negative and natural killer (NK) cell-sensitive rat MADB106 mammary adenocarcinoma (Yirmiya et al. 1992). In this study, male Fischer 344 rats were administered only one alcohol dose (1.5 to 3.5 g ethanol/kg body weight into the peritoneal cavity) 1 hour before intravenous tumor inoculation. The higher ethanol doses (i.e., 2.5 g/kg and 3.5 g/kg) significantly increased the number of lung metastases, whereas the lowest dose (1.5 g/kg) did not. Administration of naltrexone, an opioid receptor antagonist used to treat alcohol dependence, did not modify the alcohol-related increase in metastasis.
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Which Cancers Are Most at Risk From Drinking Alcohol?
And because of the study’s nature, it can also create certain “biases” in the data that may affect its accuracy or how relevant it is to the larger population of people with cancer and long-term survivors. Understanding these risks would lead to more fully informed decisions about alcohol use among individuals and families, including cancer survivors and those with a family cancer history. Noelle LoConte, M.D., an oncologist at the University of Wisconsin-Madison who studies alcohol and cancer risk, said that these findings confirm what doctors how to quid salvia have long observed. The oxidative metabolism of ethanol to acetaldehyde by alcohol dehydrogenase (ADH), and at high blood alcohol concentrations by ethanol-inducible cytochrome P4502E1 (CYP2E1) and catalase, also appears to play a role in carcinogenesis (10). The induction of CYP2E1 can activate procarcinogens, leading to the formation of reactive oxygen species which react with cellular lipids to form mutagenic DNA adducts, and DNA damage (10). Acetaldehyde can interfere with DNA synthesis and repair, form DNA-adducts, and cause cytotoxicity and mutagenicity (10).
9. Confirming the Causal Relation Reported in Observational Studies
Thus, in a related study these researchers found that administration of 2.5 g/kg ethanol 24 hours before or after tumor inoculation did not affect lung metastasis (Ben-Eliyahu et al. 1996). Yirmiya and colleagues (1992) also administered ethanol in a liquid diet for 2 weeks before and 3 weeks after tumor inoculation and found that lung metastases were increased. The interactions between alcohol use/abuse, the antitumor immune response, tumor growth, and spread of cancer are complex. A negative impact of alcohol on the immune system can lead to increased cancer mortality; however, studies also indicate that alcohol, generally in low doses, can have beneficial effects on mortality, depending on the cancer. Clearly, more mechanistic research is needed to define the complex interactions between cancer and alcohol.
Since women rarely drink alcohol in China, the main analysis focused on men, a third of whom drank regularly (most weeks in the past year). “If you’re pouring it yourself, a lot of people may not be [doing things like] using a shot glass to make a mixed drink at home. That’s a major concern with excessive alcohol consumption, that people aren’t honest with themselves,” said Dr. Abnet.
The effect of alcohol consumption on the incidence as well as the mortality of patients with prostate cancer was evaluated in a prospective cohort study of 194,797 men from the United States aged 50–71 years in 1995–1996 (Watters et al. 2010). The incidence of nonadvanced prostate cancer increased with increasing number of drinks per day, with a 25 percent increase in risk observed after high alcohol consumption (six or more drinks per day). However, an inverse correlation existed between alcohol consumption and deaths from prostate cancer, suggesting that alcohol consumption likely does not affect advanced or fatal prostate cancer. The meta-analysis by WCRF did not find an increased risk of pancreatic cancer per 10 g alcohol per day (RR 1.00 (95% CI 0.99–1.01)) but there was a possible threshold effect of increased risk for intakes of around 60 g per day (RR 1.17 (95% CI 1.05–1.29)) [7].
Basal cell carcinoma—a type of skin cancer—is the most common cancer in humans and continues to increase in incidence. Although the cure rate is high and mortality and morbidity rates are low, aggressive basal cell carcinomas are not rare. In a Spanish study, a significant positive association existed between moderate (5 to 10 drinks per week) and high (more than 10 drinks per week) alcohol consumption and the presence of aggressive basal cell carcinomas (Husein-Elahmed et al. 2012).
While studies have provided evidence on alcohol’s carcinogenic potential, further understanding of alcohol’s pathways to cancer development will inform the direction of future research. This information is useful to corroborate existing evidence, develop chemoprevention strategies, and could improve cancer therapy, but there is already a wealth of evidence to support the need for further alcohol control and cancer prevention efforts. We have discussed evidence on mechanistic and epidemiological research in the field, and this information must be used to decrease the burden of cancers, as well as other diseases and injuries, attributable to alcohol. With the immune system being compromised, alcohol consumption can exacerbate damage from viral infections such as hepatitis C virus, which is common among chronic alcoholic liver disease patients [43]. In addition, heavy episodic alcohol use might reduce the immune system’s defence against infection by disrupting the production of pro-inflammatory cytokines and increasing the expression of anti-inflammatory cytokines [33]. This is contrary to the increased expression of pro-inflammatory cytokines due to chronic alcohol exposure as discussed with other evidence on alcohol-induced inflammation (Section 3.3).
A large body of literature indicates that alcohol consumption modulates many aspects of the innate and adaptive immune systems. Alcohol originally was described as immunosuppressive, and numerous studies support the immunosuppressive aspects of alcohol consumption on the innate and adaptive immune systems. However, it also is well documented that chronic alcohol administration can activate the immune system—especially dendritic cells, T cells, and NKT cells—in experimental animals as well as humans (Cook et al. 1991; Laso et al. 2007; Song et al. 2002; Zhang and Meadows 2005).
How does alcohol affect the risk of cancer?
- The results showed that cells exposed to different concentrations of ethanol from 0.1 percent to 0.5 percent exhibited increased migration, as did cells exposed to estrogen (20 nM).
- The study detected no substantial or consistent effect of alcohol on the size or incidence of pulmonary metastases.
- However, a possible threshold effect was observed in the non-linear dose-response analysis by WCRF, where less than 45 g alcohol per day did not significantly increase the risk of liver cancer.
- Alcoholic drinks contain ethanol, which is a known carcinogen, and there are several ways in which it may cause cancer.
- The U.S. Community Preventive Services Task Force’s (CPSTF) Guide to Community Preventive Services (54), and WHO’s 2010 Global Strategy to Reduce the Harmful Use of Alcohol(8) describe a range of evidence-based alcohol control policies.
More research is needed to better understand alcohol use among people with cancer, the study team wrote. To conduct the study, the researchers used data from more than 15,000 people with a history of cancer who were participating in the National Institutes of Health All of Us Research Program. As ROS are highly reactive, their presence can lead to lipid peroxidation producing aldehydes which can bind to DNA forming etheno-DNA adducts [29,30]. These ethe-DNA adducts, namely 1,N6-ethenodeoxyadenosine and 3,N4-ethenodeoxycytidine, are highly mutagenic as they lead to mutations in several genes involved in key cell cycle regulation and tumour suppression [21]. A person’s risk of alcohol-related cancers is influenced by their genes, specifically the genes that encode enzymes involved in metabolizing (breaking down) alcohol (27). A serving of alcohol is measured by volume, but the amount of alcohol in a serving can vary greatly depending on the variety or brand of beer or wine or the type of mixed drink or cocktail—as well as how much is poured.
Why Aren’t People Aware of the Cancer Risk From Drinking?
New data from a large-scale genetic study led by Oxford Population Health confirms that alcohol directly causes cancer. The estimates of cancer cases attributed to alcohol may have been higher if past consumption had been accounted for, Dr. Abnet said. WHO had previously released alcohol policy recommendations as part of its “best buys” campaign to help countries focus on the most effective initiatives to prevent noninfectious diseases. For alcohol-related diseases, these included higher sales taxes on alcohol, limits on where and when alcohol can be purchased, and restrictions on marketing to the public. The WHO researchers also created an interactive website where people can explore the results by country, cancer site, and other variables.
It was also unclear whether alcohol is linked to other types of cancer, including lung and stomach cancers. Nearly 750,000 cases of cancer diagnosed worldwide in 2020, or 4%, can be attributed to alcohol consumption, according to a new study from the World Health Organization (WHO). While heavy drinking accounted for the most cases, light how to make myself pee and moderate drinking accounted for more than 100,000 of those cases, the study found. In the study, many people being treated for cancer and longer-term cancer survivors reported regularly drinking alcohol—many moderately, but some also heavily and often. According to the study’s findings, male long-term survivors and younger people being treated for cancer were among those who were particularly likely to be heavy or frequent drinkers.
Alcohol intake may deplete folate levels, or indeed be a cause of folate and B vitamin deficiency if alcohol constitutes the majority of calories consumed, as observed in malnourished alcoholics [21,26]. Folate deficiency affects the availability of nucleotides needed for DNA synthesis leading to accumulation of deoxyuridine monophosphate which is incorporated into new DNA molecules causing double-strand breaks and chromosomal damage [25]. Interestingly, there is evidence that higher folate intake among alcohol drinkers may attenuate the increased risk of liver cancer mortality compared with those with low folate intake [36]. This attenuation was also observed for risk of postmenopausal breast cancer among women who drink alcohol and have higher folate levels [37]. The effect of alcohol on one-carbon metabolism and folate might also be important in colorectal cancer development [20].
Drinking alcohol even at lower levels of intake can increase the risk of cancer and we previously estimated that over 100,000 cases of cancer in 2020 were caused by light and moderate drinking of the equivalent of around one or two alcoholic drinks per day [1]. Despite this, there is low public awareness of the causal link between alcohol and cancer and alcohol use is growing in several regions of the world [2,3]. Drinking alcohol increases the risk of several cancer types, including cancers of the upper aerodigestive tract, liver, colorectum, and breast. In this review, we summarise the epidemiological evidence on alcohol and cancer risk and the mechanistic evidence of alcohol-mediated carcinogenesis. There are several mechanistic pathways by which the consumption of alcohol, as ethanol, is known to cause cancer, though some are still not fully understood. Ethanol’s metabolite acetaldehyde can cause DNA damage and block DNA synthesis and repair, whilst both ethanol and acetaldehyde can disrupt DNA methylation.
