ROS accumulation leads to the upregulation of vascular endothelial growth factor (VEGF) and monocyte chemotactic protein-1 (MCP-1) [88], key mediators of tumor angiogenesis and metastasis. ROS mediated increase in the expression of metalloproteinases, MMP2 and MMP9, leads to breakdown of extracellular matrix, cell motility and thus favors tumor metastasis [89]. ROS mediated DNA damage and other effects of ROS are widely accepted as a cause for initiation and progression of breast cancer [90], HCC [88], lung cancer [91], and prostate cancer [92]. In vivo studies using mice and rats have shown that chronic alcohol consumption induces expression of pro-inflammatory cytokines and chemokines in white adipose tissue [51,52,53]. 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.
Alcohol could increase your risk of these 7 cancers
The National Cancer Institute estimates that more than 300,000 women will be diagnosed with breast cancer and 42,250 will die in the U.S. this year. Incidence rates have been creeping up about 1% a year, while death rates have been falling a little more than 1% a year. “We’re not being honest with people,” said breast cancer surgeon Laura Esserman, director of the University of California San Francisco Breast Care Center, who was not involved with the research. New research makes the case for educating women in their 40s — who’ve been caught in the crossfire of a decades-long debate about whether to be screened for breast cancer with mammograms — about the harms as well as the benefits of the exam. Finally, a reduction in inflammation from GLP-1 drugs may help lower cancer risk since cancer is a “pro-inflammatory state,” Poddar says. Human studies are messy in terms of all the possible variables that can interfere with identifying effects in observational studies, but more animal studies could help “tease out some of these different factors and control for them,” Murphy says.
Alcohol and Immune Interactions in Animal Models of Cancer
Alcohol can interact with certain chemotherapy drugs, worsen side effects, and affect liver function, which is crucial for metabolizing chemotherapy drugs. Some people have variants in different genes, such as the alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) genes. That might mean teaching doctors around the world to talk about alcohol use as a possible cause when a patient complains of sleep or memory problems or when they have the beginning signs of liver disease. “You tailor the information to the personal concerns of the patient in front of you,” says Justice.
Alcohol and Cancer Risk
An MR analysis by Ong and colleagues found no significant increase in breast cancer risk per genetically predicted drink per day (odds ratio 1.00 (95% CI 0.93–1.08)) [19]. 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. 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].
Effects of Alcohol on Tumor Growth, Metastasis, Immune Response, and Host Survival
- The outcome of in vivo experiments on alcohol and cancer development depends to a large extent on the type of carcinogen, its dose, duration of exposure, and the route of alcohol administration.
- The study detected no substantial or consistent effect of alcohol on the size or incidence of pulmonary metastases.
- Alcohol can interact with certain chemotherapy drugs, worsen side effects, and affect liver function, which is crucial for metabolizing chemotherapy drugs.
- In addition, mammography can give women a false sense of security, she said, like it did for Olivia Munn.
An increased risk of prostate cancer was observed for light and moderate drinking in Bagnardi and colleagues’ meta-analysis but not in the dose-response analysis of one drink per day by WCRF [7,8]. Wang and colleagues (2012) examined the effect of ethanol on the growth of the aggressive estrogen receptor–positive E0771 mouse mammary cancer in female C57BL/6 mice. The mice were given 2 percent ethanol in drinking water for half a day on each of 3 consecutive days before the E0771 tumor cells were inoculated into breast tissue (i.e., secondary mammary fat pad), and the ethanol feeding regimen then was continued for 24 days. The study found that the ethanol group exhibited higher primary tumor growth rates, increased final tumor weights, and a twofold increase in lung metastases compared with the water-drinking control group. Immunohisto-chemical analyses of the mammary tumor tissues also showed a higher density of tiny blood vessels in the ethanol group, indicating that ethanol promoted tumor 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. Other studies focused more on the invasion and migration in vitro of estrogen receptor–positive and estrogen receptor–negative human breast cancer cells. One study (Ma et al. 2003) compared the effects of incubation in 0.4 percent w/v ethanol for 48 hours on various breast cancer cell lines.
“The high prevalence of cancer survivors engaged in hazardous drinking highlights the need for immediate interventions,” they 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. 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). There is mounting evidence that alcohol can negatively affect one-carbon metabolism which is essential for DNA methylation and DNA synthesis [25]. Ethanol and acetaldehyde can reduce the activity of enzymes involved in one-carbon metabolism that regulate DNA methylation, namely methionine synthase, methionine adenosyl transferase and DNMT, thus dysregulating epigenetic patterns and resulting in DNA hypomethylation [20].
Although prior research suggests that the more alcohol a person consumes, the higher their risk of cancer, recent studies suggest that even relatively low amounts of drinking could increase a person’s risk. Some studies indicate that compounds in red wine, such as resveratrol, https://sober-home.org/ may have health benefits. However, these possible benefits do not outweigh the risks of alcohol consumption in regards to cancer risk. And as a physician, she thinks about the things she can say individually to a patient, one on one, to encourage them to reduce their drinking.
Much research regarding the role of the immune response in oncogenesis has centered on hepatocellular cancer (for excellent recent reviews, see Aravalli 2013; Stauffer et al. 2012; Wang 2011). However, less is known regarding the role and interaction among alcohol consumption, immune modulation of tumor growth, blood vessel formation (i.e., angiogenesis), metastasis, and survival. It is well established that immunosurveillance by the innate and adaptive immune systems plays important roles in the prevention of cancer and in controlling cancer survival (Fridmann et al. 2012; Rocken 2010). However, direct or indirect interactions of the tumors with their microenvironment can facilitate immune evasion so that the tumor is not detected by the immune system and thus can spread uncontrolled.
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). To control for this possibility, the investigators included separate analyses for men and women in their statistical models, where feasible.
Two readers, who received no information on the names and affiliations of the authors of each study or the alcohol-related results, independently determined the eligibility of each article for inclusion in the meta-analysis. When the results of a study were published in more than one article, only the most recent and complete article was included in the analysis. Because the JAMA Network Open study only looked at who was prescribed certain medications, it was not possible to determine whether patients filled those prescriptions or how long they took the medication.
Insight into the underlying mechanisms of these interactions could lead to effective immunotherapeutic approaches to treat alcoholics with cancer. Defining the epigenetic mechanisms that modulate cancer progression also has great potential for the development of new treatment options not only for treating alcoholics with cancer but also for treating other alcohol-induced diseases. In terms of risk assessment, this meta-analysis confirms that high levels of alcohol consumption (i.e., more than four drinks per day) https://sober-home.org/alcohol-detox-diet-eating-healthy-during-alcohol/ result in a substantial risk of cancer development at several sites. At the same time, other studies have shown that moderate alcohol consumption can have protective effects against certain types of heart disease. Accordingly, one must determine whether moderate alcohol consumption results in an overall favorable or unfavorable risk-benefit balance for the individual drinker or an entire population. This balance depends on the age, gender, and baseline disease rates among the members of a given population.
Country liquor is known by various names such as desi daru, tharra, toddy, tari and arrack and contains about 33 per cent (w/v) ethanol8. 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. 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).
The innate immune response rapidly identifies cancerous and/or precancerous cells and destroys them. This response is recognized by inflammatory mediators (chemokines and cytokines) produced by an array of immune cells, such as natural killer (NK) cells, macrophages, neutrophils, and dendritic cells (DCs) [7]. Upon activation, NK cells produce cytokines and chemokines that generate inflammatory responses and activate adaptive immune response. Macrophages and neutrophils possess both anti-tumor activity as well as immune suppressive activity against tumor cells. DCs act as a connecting link between the innate and the adaptive wing of the immune system by identifying and presenting foreign molecules (i.e., antigens) to other immune cells. Genetically engineered mouse models mimic pathophysiological and molecular features of human carcinogenesis [109].
Accordingly, the cessation or moderation of tobacco and/or alcohol use could avoid the majority of these cancer cases. Gu and colleagues (2005) assessed the effects of alcohol on human HT1080 colon cancer cells in a chick embryo model, focusing on variables related to the blood supply of the tumor. One of the variables analyzed was the expression of vascular endothelial growth factor (VEGF)—a growth factor that promotes blood vessel formation (i.e., is proangiogenic) and enhances tumor vascularization. Exposure of isolated tumor cells to 10 mM and 20 mM ethanol for 19 hours also increased VEGF mRNA and protein expression. The increased intratumoral vascular volume strongly correlated with the increase in tumor volume as well as with intratumoral connective tissue volume density. Finally, invasion of HT1080 cells from the tumor into blood vessels (i.e., intravasation), which occurs during metastasis, increased more than eightfold in response to ethanol.
Previously, she wrote for USA Today, where she was selected to help launch the newspaper’s wellness vertical. “We know it’s tough to stop smoking. It’s easier to never start smoking in the first place. So I would say a report like this should just emphasize that people give them incentive to say, ‘You know what, I’m never going to start smoking,'” he said. We help leaders and future leaders in the healthcare industry work smarter and faster by providing provocative insights, actionable strategies, and practical tools to support execution. Separately, this expert insight explains three strategies organizations can use to leverage oncology pharmacists and improve cancer care. Similarly, these ready-to-use slides outline the major structural shifts impacting cancer care, as well as the strategic decisions that oncology leaders will need to make.
The foundation notes drinks with zero or little alcohol content are gaining popularity in Australia. “Our research shows that zero alcohol products and marketing are likely making young people more familiar with alcohol brands and further normalising alcohol consumption,” he said. More than half of teenagers aged 15 to 17 surveyed for the research found zero alcohol drink packaging attractive. The Australian Cancer Council has raised alarm bells about zero-alcohol drinks following research into their impact on teenagers.
Acetaldehyde can interfere with DNA synthesis and repair, form DNA-adducts, and cause cytotoxicity and mutagenicity (10). As with most questions related to a specific individual’s cancer treatment, it is best for patients to check with their health care team about whether it is safe to drink alcohol during or immediately following chemotherapy treatment. The doctors and nurses administering the treatment will be able to give specific advice about whether it is safe to consume alcohol while undergoing specific cancer treatments. In addition to its involvement in downstream ROS-producing pathways, it is hypothesised that IL-8 contributes to further accumulation of white blood cells (neutrophils, specifically) in the liver leading to acute inflammation. Elevated IL-8 levels have been found in patients with acute liver injury such as alcoholic hepatitis [34].