However, additional studies are warranted, because estrogen receptor–negative breast cancer generally is more aggressive, and patients how to store a urine sample have a worse prognosis than patients with estrogen receptor–positive breast cancer. Moreover, conversion from estrogen receptor alpha positive to estrogen receptor alpha negative can occur (Hoefnagel et al. 2010). The most common histological subtype of liver cancer is hepatocellular carcinoma (HCC) and around 154,700 cases of HCC in 2020 were attributable to alcohol consumption [1]. When restricted to HCC only, meta-analysis of WCRF sources resulted in a 14% increased risk of HCC (RR 1.14 (95% CI 1.04–1.25)) per 10 g alcohol per day [7]. 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.

Alcohol and Cancer: Epidemiology and Biological Mechanisms

This was similar to the findings of Bagnardi and colleagues where light or moderate drinking did not significantly increase liver cancer risk but risk among heavy drinkers doubled (RR 2.07 (95% CI 1.66–2.58)) [8]. The data suggest that inhibition of NK-cell cytolytic activity in mice consuming 20 percent ethanol does not lead to enhanced metastasis following inoculation of B16BL6 melanoma. This lack of interaction between alcohol consumption and NK-cell cytolytic activity in B16BL6 melanoma lung metastasis was further confirmed in another strain of mice (i.e., beige mice) that naturally have low NK cytolytic activity (Spitzer et al. 2000). In other experiments to determine how ethanol decreases metastasis of B16BL6 melanoma, either isolated tumor cells grown in the presence of 0.3 percent ethanol or tumor cells from alcohol-consuming mice were inoculated into water-drinking mice (Blank and Meadows 1996). Mice that had received either tumor cells cultured in the presence of ethanol or derived from mice drinking 20 percent alcohol showed increased lung metastasis compared with control mice or those receiving tumor cells derived from mice drinking 10 percent ethanol. However, because alcohol drinking inhibits metastasis, there seem to be other factors induced by ethanol that counter this metastatic potential.

Why Aren’t People Aware of the Cancer Risk From Drinking?

Numerous changes need to be made to raise public awareness of the fact that drinking alcohol raises the risk of several types of cancer. The investigators also analyzed the levels of the various types of blood cells in the spleen (Zhang et al. 2012). The spleen contains proportionally more B cells and fewer T cells than the peripheral blood; among the T cells, the spleen normally contains a higher proportion of CD8+ T cells than the peripheral blood. The analyses found that alcohol consumption also led to a decrease in CD8+ T cells in the spleen; however, this reduction was less remarkable than in peripheral blood. Furthermore, alcohol consumption reduced the overall numbers of B cells in the spleen, although it did not affect all types of B cells equally. Thus, there was no effect on splenic follicular B cells, whereas the number of immature T1 B (CD19+CD93+CD23−) cells increased and the number of marginal zone B cells (CD19+CD1dhiCD21hi) decreased.

Men accounted for roughly 75% of the alcohol-related cancer cases—or 568,700 total cases—while women accounted for the remaining  172,600 cases. According to the study, cancers of the esophagus (189,700 cases), liver (154,700 cases), and breast (98,300 cases) "contributed the most cases." The COVID-19 pandemic also appears can alcoholics eat food cooked with alcohol to have caused a spike in drinking among women in the United States and elsewhere, explained Dr. LoConte. “Getting access to alcohol has gotten a lot easier, with things like delivery and drive-through pickup, and women in particular are bearing a huge burden of caregiving, which has led to more drinking,” she said. Overall, eastern Asia and central and eastern Europe had the highest proportions of cancer cases attributed to alcohol consumption, and northern Africa and western Asia had the lowest. Trends for women differed slightly, with the highest proportions of cancer cases attributed to alcohol consumption found in central, eastern, and western Europe; Australia; and New Zealand.

How does the combination of alcohol and tobacco affect cancer risk?

Cancers of the upper aerodigestive tract can also be characterised as having a more than multiplicative increased risk when alcohol and tobacco are consumed together. For oesophageal squamous cell carcinoma, a cohort study in the Netherlands observed an eight times risk among current smokers who drank 15 g alcohol or more per day, compared with never smokers who consumed less than 5 g alcohol per day [12]. The effects of alcohol consumption on cancer risk have been studied for many decades and an mescaline benefits association with alcohol has been observed for multiple cancer sites.

1. The study had several limitations, including that it only looked at current alcohol consumption, not past drinking habits, said Dr. Abnet.
2. Ethanol’s metabolite acetaldehyde can cause DNA damage and block DNA synthesis and repair, whilst both ethanol and acetaldehyde can disrupt DNA methylation.
3. Inflammation is a key pathway to cancer progression at several sites and is enhanced by alcohol use.
4. More-over, the numbers of lung metastases in the ethanol-drinking mice were significantly lower at 21 days.
5. Another study published in 2021 showed that nearly 70% of people did not even know that alcohol was a cancer risk factor.

In that study, a molecule that can inhibit VEGF receptor 2 blocked alcohol’s stimulatory effect on tumor growth, indicating that alcohol acts via a VEGF pathway. 3Interestingly, the same cell type was decreased in the peripheral blood in the cancer patients compared with control patients. 1In estrogen-positive breast cancer, the cancer cells carry the estrogen receptor and depend on estrogen for growth. In contrast, in triple-negative breast cancer, the cancer cells carry neither estrogen nor progesterone or HER2 receptors. Interpersonal influences, including interactions with family and friends, also shape knowledge and behaviors (42, 43).

Alcohol is estimated to account for 6% of cancer cases in the U.S. — more than 75,000 per year — and nearly 19,000 cancer deaths, according to the American Cancer Society. Alcohol is the third biggest controllable risk factor for the disease, after tobacco smoking and excess weight. Other investigators (Kushiro and Nunez 2012) found that B16BL6 melanoma cells grown in 0.1 percent, 0.2 percent, or 0.5 percent ethanol showed considerably reduced cell invasion and, at the highest ethanol concentration, reduced cell motility and anchorage-dependent growth. In addition, the highest ethanol dose altered the expression of several genes that play prominent roles in regulating melanoma metastasis (i.e., the IL6, Nfkb, snail1, E-cadherin, Kiss1, Nm23-m1, and Nm23-m2 genes). Alcohol consumption is a well-established risk factor for cancer and has been linked to cancers of the oral cavity and pharynx, oesophagus, liver, colorectum and breast.

The effect of alcohol consumption on mortality of women with breast cancer is particularly complex and seems to differ according to age, estrogen receptor status, and extent of alcohol drinking. Clearly, more breast cancer–specific studies are needed that correlate mortality with the properties of the cancer and the level of alcohol consumption. Chemokines and their receptors often are altered in cancer patients, and their importance in cancer progression has been the subject of several recent reviews (Aldinucci and Colombatti 2014; de Oliveira et al. 2014; Sarvaiya et al. 2013).

After repeated activation, however, these cells become anergic and switch to a cytokine profile that inhibits anti-tumor immune responses and favors tumor progression (i.e., a high ratio of IL-4 to IFN-γ) (Parekh et al. 2005). The invariant NKT cells from the alcohol-consuming, melanoma-bearing mice exhibit a high IL4/IFN-γ ratio, indicating that they express a cytokine profile favoring immune inhibition and tumor progression (Zhang et al. 2015). Interactions with clinicians could affect alcohol consumption behavior, as they are relatively trusted sources of health information (45). However, in a cross-sectional survey of cancer survivors, only 14% of regular drinkers recalled receiving counselling from a clinician to quit drinking, although those who did were five-fold more likely to report reducing or stopping drinking compared to those who did not receive counseling (46). These findings suggest that clinicians may underappreciate cancer risks due to alcohol, and need additional guidance to reinforce clear and consistent messaging to effectively discuss this issue with their patients.

“We need to really make sure that we reinforce the message that all alcohol increases cancer risk,” she said. 2The exception to this is a study in Russia indicating an inverse association between alcohol consumption and mortality (Zaridze et al. 2009). Despite substantial epidemiological and mechanistic evidence on alcohol and cancer, several knowledge gaps remain that if filled could improve estimates of the burden of alcohol-attributable cancers, and inform tailord interventions to reduce consumption. As a doctor, Justice said, she thinks about what she can say to a patient in a one-on-one setting to encourage them to reduce their alcohol consumption. "There's pretty good data that you can get people to decrease their alcohol consumption with brief motivational information," Justice said. The results remained the same when the data were adjusted for other cancer risk factors, such as smoking, diet, physical activity, body mass and family history of 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). Several studies examined the specific effects of ethanol on various aspects of disease progression in human breast cancer cell lines, including proliferation of cells. Singletary and colleagues (2001) found that incubation in 0.4 percent w/v ethanol increased cell proliferation in the estrogen receptor–positive MCF-7 and ZR75.1 breast cancer cells but not in the estrogen receptor–negative BT-20 and MDA-MB-231 cells.

These patients often are immunodeficient because of their alcohol abuse and heavy tobacco use; however, the contribution of continued alcohol abuse to altered immune parameters in these patients has largely not been assessed. Several studies using animal cancer models indicate tumor-specific differences in the effect of alcohol on tumor growth and metastasis. These models included various types of breast cancer, melanoma, lung cancer, colon cancer, and liver cancer (i.e., hepatocellular carcinoma).