Dendritic cells are important in presenting molecules that identify a cell as harmful or foreign (i.e., antigens) to other immune cells and are a bridge between the innate immune response and the B-cell and T-cell responses that characterize the adaptive immune system. Another enzyme, called aldehyde dehydrogenase 2 (ALDH2), metabolizes toxic acetaldehyde to nontoxic substances. Some people, particularly those of East Asian descent, carry a variant of the gene for ALDH2 that encodes a defective treatment national institute on drug abuse nida form of the enzyme. In people who produce the defective enzyme, acetaldehyde builds up when they drink alcohol. The accumulation of acetaldehyde has such unpleasant effects (including facial flushing and heart palpitations) that most people who have inherited the ALDH2 variant are unable to consume large amounts of alcohol and therefore have a low risk of developing alcohol-related cancers. There is a strong scientific consensus that alcohol drinking can cause several types of cancer (1, 2).
Alcohol, Tumor Growth, Invasion, and Metastasis in Animal Models
Overall alcohol-related mortality trends in the US were stable from 1999 to 2007 (APC, 0.0; 95% CI, −0.6 to 0.6) but increased by 3.0% per year (95% CI, 2.6%-3.5%) from 2007 to 2018 and, more recently, by 14.1% per year (95% CI, 8.2%-20.3%) from 2018 to 2020. For more information about the effects of alcohol on the heart, visit the British Heart Foundation’s website. People should consider discussing their alcohol use with a healthcare team to understand the specific implications for their treatment and overall health. Alcohol can interact with certain chemotherapy drugs, worsen side effects, and affect liver function, which is crucial for metabolizing chemotherapy drugs. However, some risks may persist, especially if there has been heavy or long-term alcohol use. Cells that are damaged by the alcohol may try to repair themselves, which could lead to DNA changes that can be a step toward cancer.
What do experts say about alcohol consumption?
Recent studies from our laboratory has reported that chronic-binge alcohol induces adipose tissue inflammation in vivo in female mice [54]. Alcohol-induced chronic inflammation in breast adipose tissue creates microenvironment that is conducive to increased tumor cell proliferation, metastasis, and enhanced tumor-related angiogenesis. Increased oxidative stress and continuous secretion of pro-inflammatory cytokines by inflamed adipocytes can elicit epigenetic changes in pre-cancerous cells [55]. It is plausible that inflamed tissue microenvironment offers an ideal setting for tumor onset and progression, and alcohol acts as a major driving force. To determine the effects of alcohol on the risk for various types of cancer, the researchers used three statistical methods.
1. Oral Cavity Pharyngeal and Laryngeal Cancers
Of those who may have been actively undergoing treatment for cancer, about 75% drank alcohol, many heavily. Research has shown that when you stop drinking, the risk for alcohol-related cancers declines over time, Bevers says. While she says some studies suggest that there are compounds in red wine that offer cardiovascular benefits, there are plenty of other ways to keep your heart healthy.
4. Liver Cancer
The curves shown here were obtained by fitting certain statistical models to the data from several studies (i.e., a meta-analysis). Blue dotted lines indicate 95-percent confidence intervals; that is, the range of RR that is 95 percent likely to show a true RR. The association between various levels of alcohol consumption and an increased risk of liver cancer remains difficult to interpret even with the pooled data used in this meta-analysis. This difficulty results from the fact that, as discussed earlier, the association between alcohol consumption and liver cancer is only indirect. Furthermore, patients with liver cancer resulting from cirrhosis typically have reduced their alcohol consumption by the time they develop liver cancer (Aricò et al. 1994). Alcoholic drinks contain ethanol, which is a known carcinogen, and there are several ways in which it may cause cancer.
Metastasis did occur, however, in the draining inguinal lymph nodes in mice consuming 20 percent weight per volume ethanol for 12 weeks (Zhang et al. 2011b). For oral and oropharyngeal cancer, an MR study using genetic data on 6000 oral or oropharyngeal cancer cases and 6600 controls found a positive causal effect of alcohol consumption independent of smoking [16]. The authors concluded that previous estimates of the association between alcohol and oral and oropharyngeal cancer from observational studies may have been underestimated [16]. Another MR study on UK Biobank data found that drinking alcohol, especially above the UK’s low-risk guideline of up to 14 units per week, was causally related with head and neck cancers, but not breast cancer [17].
Epidemiology and biology of alcohol and cancer risk
Almost every tribe has a unique way of preparing alcoholic beverages using locally available plant components as starter cultures9. Mizoram and Meghalaya have reported a higher prevalence of alcohol use in comparison to other northeastern States as per the fourth round of district-level household survey10. Alcohol can raise the levels of estrogen, a hormone important in the growth and development of breast tissue. Drinking alcohol can also lead to oxidative stress in cells, causing them to create more reactive oxygen species (chemically reactive molecules that contain oxygen).
More than 100 empirical studies have established a positive correlation between moderate or chronic ethanol consumption and the incidence of breast cancer in pre- and post-menopausal women [44]. It has been reported that alcohol intake of more than 27 drinks per week increases breast cancer risk in pre-menopausal women irrespective of the type of alcoholic beverage consumed [44]. Among post-menopausal women, consumption of more than six drinks per week increases breast cancer risk. The association between alcohol and breast cancer is attributed to the increased levels of estrogen in women consuming alcohol. Other plausible mechanisms include enhanced mammary gland susceptibility to carcinogenesis, increased mammary carcinogen DNA damage, and greater metastatic potential of breast cancer cells [6].
Following epidemiological evidence of the link between alcohol use and risk of cancer at multiple sites, several pathways have been investigated to explain the carcinogenic effects of alcohol. Here, we discuss alcohol detox and rehab programs the key mechanisms linking alcohol consumption to carcinogenesis, which are depicted in Figure 4. The innate immune response rapidly identifies cancerous and/or precancerous cells and destroys them.
- New data from a large-scale genetic study led by Oxford Population Health confirms that alcohol directly causes cancer.
- Although extensive epidemiologic evidence links the etiology of cancer to alcohol, very little information addresses the critical question of whether and how alcohol modulates tumor metastasis, survival, and the response to cancer therapy.
- The increased intratumoral vascular volume strongly correlated with the increase in tumor volume as well as with intratumoral connective tissue volume density.
- Decreased NK cytolytic activity has also been reported in human cancers, including HNC, breast, colorectal and prostate cancer [137,138].
The effect of ethanol on mammary cancer growth has been studied in a number of animal models, using both rodent and human tumor cell lines. Given the study’s findings, “there’s also a need to better understand why so many cancer survivors have such high alcohol consumption,” she continued. Greater collaboration with other specialties and clinicians who regularly interact with people with cancer, such as oncology nurses, to develop ways to reduce risky drinking behaviors will be needed moving forward, Dr. Agurs-Collins said. At the moment, however, proven ways to help people with cancer limit drinking during or after completing treatment are extremely limited, Dr. DuVall said.
Here, we discuss evidence from large meta-analyses of observational studies and emerging evidence from Mendelian randomisation studies. Evidence is strongest for North America and Europe, where more studies have been conducted, but other regions also show some evidence of a similar association. Much additional research has been done regarding the details of the alcohol consumption (e.g., beverage type, drinking pattern, the participant’s age at the time of consumption) and the details of the breast cancer (e.g., tumor subtype). In contrast to the extensive studies involving T cells in anti-tumor immunity, the knowledge of B cells in anti-tumor immune responses are limited and controversial. One of the studies reported that B cells enhanced T cell mediated anti-tumor immunity by producing anti-tumor antibody and presenting tumor-antigen to T cells [159].
But most Americans aren’t aware of this link, thanks to seemingly contradictory research and mixed messaging from public health experts. A study published in 2023 found widespread mistaken beliefs that how long do alcohol cravings last in recovery the risk varies by beverage type, with the lowest cancer risk assigned to wine. Another study published in 2021 showed that nearly 70% of people did not even know that alcohol was a cancer risk factor.
These experiments showed that 10 percent w/v ethanol did not affect metastasis after intravenous tumor inoculation in female C57BL/6 mice consuming alcohol for 2 weeks or spontaneous metastasis in mice injected 1 week after initiating ethanol feeding. However, lung metastasis was inhibited if intravenous injection of tumor cells occurred at 4, 6.5, 7, and 12 weeks after initiation of 20 percent w/v ethanol. Similarly, spontaneous metastasis to the lung was significantly inhibited in mice injected with melanoma at 1, 4, 6.5, and 10 weeks of consuming 20 percent ethanol. Evidence that directly implicates immune cells from both the innate and adaptive immune systems in control of cancer growth and progression continues to accumulate.
Another limitation of this and other meta-analyses is that alcohol consumption levels may have been systematically underreported in several studies, leading to biased RR estimates. Overall, the amount of alcohol someone drinks over time, not the type of alcoholic beverage, seems to be the most important factor in raising cancer risk. Most evidence suggests that it is the ethanol that increases the risk, not other things in the drink. Invasive ability generally was related to the expression of ErbB2/neu, an epidermal growth factor (EGF) receptor that is amplified in 20 to 30 percent of breast cancer patients, with higher ErbB2/neu levels indicating higher risk of lymph node metastasis and poor prognosis. More detailed studies of the relationship between alcohol, ErbB2/neu, and invasion in the human breast cancer cell line T47D found that activation of the EGF receptor by addition of EGF did not significantly affect ethanol’s ability to enhance invasiveness (Luo and Miller 2000). Conversely, prevention of ErbB2/neu production inhibited the ability of ethanol to increase migration (Luo and Miller 2000).
Recent studies show that combination of DEN followed by alcohol exposure increase incidence of HCC promoted by underlying alcoholic liver disease [99]. Experimental model of chemically induced HCC in male BALB/c mice was developed in which DEN initiation with CCl4 and ethanol promotion induced a two-stage liver carcinogenesis mimicking the usual sequence of events observed in human HCC [100]. This meta-analysis includes most published information on alcohol and cancer and, the limitations discussed above notwithstanding, consequently provides the most accurate estimates of the RRs for common cancers considered to be alcohol-related. For example, the analysis was unable to identify a threshold level of alcohol consumption below which no increased risk for cancer is evident. Furthermore, this meta-analysis found that the association of alcohol with the risk for oral and pharyngeal cancer appears to be stronger than the association with esophageal or laryngeal cancer across increasing levels of alcohol intake.