Alcohol causes cancer, and here’s the evidence:

Alcohol causes at least seven types of cancer
 

“Alcohol causes cancer, and here’s the evidence… Many of us are aware of the short-term effects of drinking too much – feeling sick, a hangover, a spot of embarrassment, a vague but hard-to-pin-down sense of guilt – but the long-term effects often slip under the radar. These include a higher risk of many cancers, heart disease, stroke and more.”   http://scienceblog.cancerresearchuk.org/2010/01/28/alcohol-and-cancer-the-evidence/   

“ALCOHOL AND CANCER… Epidemiological data have identified chronic alcohol consumption as a significant risk factor for upper alimentary tract cancer, including cancer of the oropharynx, larynx and the oesophagus and of the liver.” http://alcalc.oxfordjournals.org/content/39/3/155.long

“Molecular mechanisms of alcohol-mediated carcinogenesis… Although the mechanisms for alcohol-associated carcinogenesis are not completely understood, most recent research has focused on acetaldehyde, the first and most toxic ethanol metabolite, as a cancer-causing agent. Ethanol may also stimulate carcinogenesis… Alcohol-related carcinogenesis may interact with other factors such as smoking, diet and comorbidities, and depends on genetic susceptibility.” http://www.ncbi.nlm.nih.gov/pubmed/17646865

“Liver cancer and alcohol… Based on the association of alcohol with cancer, a International Agency for Research on Cancer working group recently deemed alcoholic beverages “carcinogenic to humans,” causally related to occurrence of malignant tumors of the oral cavity, pharynx, larynx, esophagus, liver, colorectum, and female breast.”  http://www.ncbi.nlm.nih.gov/pubmed/23101985

“Alcohol and pancreatic cancer… heavy alcohol consumption has been known to be a major cause of chronic pancreatitis and a risk factor for type 2 diabetes mellitus, both of which are linked to pancreatic cancer.”  http://www.ncbi.nlm.nih.gov/pubmed/16054982

“Alcohol drinking and colorectal cancer risk: an overall and dose–response meta-analysis of published studies… The International Agency for Research on Cancer (IARC) concluded that alcohol consumption is related to colorectal cancer (CRC)… This meta-analysis provides strong evidence for an association between alcohol drinking of >1 drink/day and colorectal cancer risk.”  http://annonc.oxfordjournals.org/content/22/9/1958.long

“Alcohol consumption and the risk of breast cancer… Epidemiologic studies addressing the association of alcohol consumption with breast cancer consistently suggest a modest association and a dose-response relationship… Data from a variety of epidemiologic studies suggest that chronic alcohol consumption even in moderate amounts increases a woman’s risk for breast cancer… Epidemiologic data further suggest that consumption of larger amounts of alcohol is associated with a higher risk of breast cancer…  Avoiding overconsumption of alcohol is recommended, especially for women with known risk factors for breast cancer.”  http://www.scielosp.org/scielo.php?script=sci_arttext&pid=S0036-36342011000500012&lng=en&nrm=iso&tlng=en 

“Alcohol consumption and digestive tract cancer…  data indicating that alcohol is an important factor increasing the risk to develop gastrointestinal cancer are consolidating… Functional genetic variants of alcohol-metabolizing enzymes proved to be associated with increased risk for esophageal and gastric cancer… Alcohol overconsumption is a serious avoidable risk factor for the development of gastrointestinal tract cancer, both alone but even more in combination with other risk factors such as tobacco and obesity.”  http://www.ncbi.nlm.nih.gov/pubmed/22797570

“Cancer stem cells generated by alcohol, diabetes, and HCV”  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3306127/

“Epidemiology and Pathophysiology of Alcohol and Breast Cancer: Update 2012… Alcohol consumption is a risk factor for cancer of various organs including the upper alimentary tract, the liver, the colorectum and the female breast… Women should not exceed one drink/day, and women at elevated risk for breast cancer should avoid alcohol or consume alcohol occasionally only.”  http://alcalc.oxfordjournals.org/content/47/3/204.long

“Human carcinogenesis and alcohol in hepato-gastroenterology… Alcohol consumption is one of the top-10 risks for worldwide burden of disease. The International Agency for Research for Cancer affirmed that there was evidence for the carcinogenicity of ethanol in animals and classified alcohol consumption as carcinogenic for humans. Alcohol consumption causes cancers of the oral cavity, pharynx, larynx, oesophagus, colorectum, liver, pancreas and female breast…”  http://www.ncbi.nlm.nih.gov/pubmed/22696879 

“The Burden of Cancer Attributable to Alcohol Consumption… All types of alcoholic beverages are associated with an increased risk which suggests that ethanol itself is the crucial compound which causes that effect… In our opinion, there are not enough data to support the actually safe intake of alcohol. Any level of alcohol consumption increase the risk of developing an alcohol related cancer.”  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3391950/ 

“Tobacco smoking, alcohol drinking and risk of oral cavity cancer by subsite: results of a French population-based case-control study, the ICARE study…  Tobacco smoking increased the risk of oral cavity cancer even for the smaller quantities and durations, whereas alcohol drinking increased this risk only in heavy drinkers who were also ever smokers. The combined effect of smoking and drinking was greater than multiplicative…”  http://www.ncbi.nlm.nih.gov/pubmed/22976386

“Alcohol-Attributable Cancer Deaths and Years of Potential Life Lost in the United States. Objectives: Our goal was to provide current estimates of alcohol-attributable cancer mortality and years of potential life lost (YPLL) in the United States. Results: Alcohol consumption resulted in an estimated 18,200 to 21,300 cancer deaths, or 3.2% to 3.7% of all US cancer deaths. Conclusions: Alcohol remains a major contributor to cancer mortality and YPLL. Higher consumption increases risk but there is no safe threshold for alcohol and cancer risk. Reducing alcohol consumption is an important and underemphasized cancer prevention strategy.”  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3673233/

“Ethanol-mediated promotion of oesophageal carcinogenesis: association with lipid peroxidation and changes in phospholipid fatty acid profile of the target tissue… Ethanol consumption is a high risk factor for oesophageal carcinoma…  ethanol may promote carcinogenesis through excessive cell proliferation…”  http://www.ncbi.nlm.nih.gov/pubmed/9199722

“Ethanol-mediated carcinogenesis in the human esophagus implicates CYP2E1 induction and the generation of carcinogenic DNA-lesions… Chronic alcohol consumption is a major risk factor for esophageal cancer… Ethanol exerts its carcinogenic effect in the liver among others via the induction of cytochrome P450 2E1 (CYP2E1) and the generation of carcinogenic etheno-DNA adducts…” http://www.ncbi.nlm.nih.gov/pubmed/20715111

“Ethanol enhances tumor angiogenesis in vitro induced by low-dose arsenic in colon cancer cells through hypoxia-inducible factor 1 alpha pathway… Arsenic has been known to induce carcinogenesis and enhance tumor development via complex and unclear mechanism. Ethanol is also a well-established risk factor for many malignancies…We conclude that ethanol is able to enhance arsenic-induced tumor angiogenesis in colorectal cancer cells…”  http://www.ncbi.nlm.nih.gov/pubmed/22872060

“Ethanol-induced mast cell-mediated inflammation leads to increased susceptibility of intestinal tumorigenesis in the APC Δ468 min mouse model of colon cancer… Chronic and frequent alcohol (ethanol [EtOH]) intake has been associated with an increased incidence of several types of cancers including breast, mouth, throat, esophageal, stomach, and colorectal (CRC). The underlying mechanism of this deleterious carcinogenic effect of alcohol has not been clearly established… Our data show that chronic alcohol intake promotes: (i) intestinal tumorigenesis and tumor invasion in genetically susceptible mice; (ii) increases in polyp-associated mast cells; and (iii) mast cell-mediated tumor migration in vitro. Both our in vivo and in vitro studies suggest that mast cell-mediated inflammation could be 1 mechanism by which alcohol promotes carcinogenesis.”  http://www.ncbi.nlm.nih.gov/pubmed/23320800

“Ethanol Promotes Chemically Induced Oral Cancer in Mice through Activation of the 5-Lipoxygenase Pathway of Arachidonic Acid Metabolism… Alcohol drinking is a known risk factor for oral cancer in humans… this study clearly demonstrated that ethanol promoted 4NQO-induced oral carcinogenesis…”  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3208736/

“Ethanol Disrupts Vascular Endothelial Barrier: Implication in Cancer Metastasis… ethanol exposure enhances tumor progression. Ethanol exposure promotes cancer cell invasion and is implicated in tumor metastasis…Our results indicate that ethanol may facilitate cancer metastasis by disrupting the vascular endothelial barrier.”  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3327869/

“Ethanol Promotes Mammary Tumor Growth and Angiogenesis: the Involvement of Chemoattractant Factor MCP-1… Alcohol consumption is a risk factor for breast cancer in humans. Experimental studies indicate that alcohol exposure promotes malignant progression of mammary tumors… Ethanol promotes mammary tumor growth and metastasis… A causal role was recently attributed to inflammation in many malignant diseases, including breast cancer… It has been demonstrated that alcohol induces pro-inflammatory mediators, and enhanced inflammation may underlie many diseases or disorders caused by alcohol abuse…”  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3323664/

“Alcohol drinking, consumption patterns and breast cancer among Danish nurses: a cohort study… these data suggest, that weekly alcohol consumption increases the risk of breast cancer in women reporting alcohol consumption above the average for women in general. The risk is minor for moderate levels of weekly alcohol intake, but increases for each extra drink consumed. Weekend consumption and binge drinking seem to be related to an additional increased risk of breast cancer.”  http://eurpub.oxfordjournals.org/content/17/6/624.long

“Alcohol intake, type of beverage, and risk of breast cancer in pre- and postmenopausal women… Most studies of the relation between alcohol consumption and breast cancer have shown a modestly increased risk… CONCLUSIONS: Total alcohol intake of more than 27 drinks per week increases breast cancer risk in premenopausal women independently of the type of alcohol. Among postmenopausal women, an intake of spirits of more than six drinks per week increases breast cancer risk.”  http://www.ncbi.nlm.nih.gov/pubmed/15252295

“Moderate alcohol consumption during adult life, drinking patterns, and breast cancer risk… Relative risks of developing invasive breast cancer… Low levels of alcohol consumption were associated with a small increase in breast cancer risk, with the most consistent measure being cumulative alcohol intake throughout adult life. Alcohol intake both earlier and later in adult life was independently associated with risk… higher consumption of alcohol has been associated with an increased risk of breast cancer…”  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3292347/

“Moderate alcohol consumption and breast cancer in women: from epidemiology to mechanisms and interventions… Epidemiologic studies indicate that moderate alcohol consumption increases breast cancer risk in women… In this commentary, we focus on some recent epidemiologic studies linking moderate alcohol consumption to breast cancer risk and place the results of those studies within the framework of our current understanding of the temporal and mechanistic basis of human carcinogenesis. This analysis supports the hypothesis that alcohol acts as a weak cumulative breast carcinogen and may also be a tumor promoter.”  http://www.ncbi.nlm.nih.gov/pubmed/23072454

“Light alcohol drinking and cancer: a meta-analysis… There is convincing evidence that alcohol consumption increases the risk of cancer… We evaluated the association between light drinking and cancer of the colorectum, breast, larynx, liver, esophagus, oral cavity and pharynx… CONCLUSIONS: Light drinking increases the risk of cancer of oral cavity and pharynx, esophagus and female breast.”  http://www.ncbi.nlm.nih.gov/pubmed/22910838

“Alcohol-related diseases and carcinogenesis…  Data are presented demonstrating the induction, by chronic ethanol consumption, of microsomal enzymes which convert procarcinogens to carcinogens… The hypothesis is presented that ethanol-mediated induction of enzyme systems which activate procarcinogens to carcinogens in various tissues contributes to the enhanced incidence of cancer in the alcoholic.”  http://www.ncbi.nlm.nih.gov/pubmed/221110

“The Role of Cytochrome P450 2E1 in Ethanol-Mediated Carcinogenesis… there is increasing evidence that CYP2E1 induced by chronic alcohol consumption plays an important role in alcohol mediated carcinogenesis.”  http://www.ncbi.nlm.nih.gov/pubmed/23400919 

Amphiregulin is a factor for resistance of glioma cells to cannabinoid-induced apoptosis.

“Gliomas, one of the most malignant forms of cancer, exhibit high resistance to conventional therapies. Identification of the molecular mechanisms responsible for this resistance is therefore of great interest to improve the efficacy of the treatments against these tumors. Delta9-Tetrahydrocannabinol (THC), the major active ingredient of marijuana, and other cannabinoids inhibit tumor growth in animal models of cancer, including glioma, an effect that relies, at least in part, on the ability of these compounds to induce apoptosis of tumor cells.

…we identified the epidermal growth factor receptor ligand amphiregulin as a candidate factor to mediate the resistance of glioma cells to cannabinoid treatment… in vivo silencing of amphiregulin rendered the resistant tumors xenografts sensitive to cannabinoid antitumoral action.

Amphiregulin expression was associated with increased extracellular signal-regulated kinase (ERK) activation, which mediated the resistance to THC by blunting the expression of p8 and TRB3-two genes involved in cannabinoid-induced apoptosis of glioma cells.

 Our findings therefore identify Amphirregulin as a factor for resistance of glioma cells to THC-induced apoptosis and contribute to unraveling the molecular bases underlying the emerging notion that targeted inhibition of the EGFR pathway can improve the efficacy of antitumoral therapies.”

http://www.ncbi.nlm.nih.gov/pubmed/19229996

Stimulation of the midkine/ALK axis renders glioma cells resistant to cannabinoid antitumoral action

“Δ9-Tetrahydrocannabinol (THC), the major active ingredient of marijuana, and other cannabinoids inhibit tumor growth in animal models of cancer, including glioma, an effect that relies, at least in part, on the stimulation of autophagy-mediated apoptosis in tumor cells. 

…Altogether, our findings identify Mdk as a pivotal factor involved in the resistance of glioma cells to THC pro-autophagic and antitumoral action, and suggest that selective targeting of the Mdk/ALK axis could help to improve the efficacy of antitumoral therapies for gliomas.”

Full text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3131933/

Stimulation of ALK by the growth factor midkine renders glioma cells resistant to autophagy-mediated cell death

“Δ9-tetrahydrocannabinol (THC), the main active component of marijuana, promotes cancer cell death via autophagy stimulation.

We find that activation of the tyrosine kinase receptor ALK by its ligand midkine interferes with the signaling mechanism by which THC promotes autophagy-mediated glioma cell death.”

 http://www.ncbi.nlm.nih.gov/pubmed/21593591

Marijuana Chemical May Fight Brain Cancer – CBSNews

“The active chemical in marijuana promotes the death of brain cancer cells by essentially helping them feed upon themselves, researchers in Spain report.

Guillermo Velasco and colleagues at Complutense University in Spain have found that the active ingredient in marijuana, THC, causes brain cancer cells to undergo a process called autophagy. Autophagy is the breakdown of a cell that occurs when the cell essentially self-digests.

The team discovered that cannabinoids such as THC had anticancer effects in mice with human brain cancer cells and people with brain tumors . When mice with the human brain cancer cells received the THC, the tumor growth shrank.

Two patients enrolled in a clinical trial received THC directly to the brain as an experimental treatment for recurrent glioblastoma multiforme , a highly aggressive brain tumor. Biopsies taken before and after treatment helped track their progress. After receiving the THC, there was evidence of increased autophagy activity.

The findings appear in the April 1 issue of the Journal of Clinical Investigation.

The patients did not have any toxic effects from the treatment. Previous studies of THC for the treatment of cancer have also found the therapy to be well tolerated, according to background information in journal article.

Study authors say their findings could lead to new strategies for preventing tumor growth.”

http://www.cbsnews.com/2100-500368_162-4913095.html

“Cannabinoid action induces autophagy-mediated cell death through stimulation of ER stress in human glioma cells…These findings describe a mechanism by which THC can promote the autophagic death of human and mouse cancer cells and provide evidence that cannabinoid administration may be an effective therapeutic strategy for targeting human cancers.” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2673842/

 

Structure-dependent inhibitory effects of synthetic cannabinoids against 12-O-tetradecanoylphorbol-13-acetate-induced inflammation and skin tumour promotion in mice.

“Whether and how synthetic cannabinoids affect inflammation and carcinogenesis has not been well studied. The present study was thus conducted to assess effects of synthetic cannabinoids on inflammation and carcinogenesis in vivo in mice…

The present results suggest that synthetic cannabinoids, such as JWH-018, -122 and -210, may be used as cancer chemopreventive agents in the future.”

http://www.ncbi.nlm.nih.gov/pubmed/23837590

Drug War Blocking Potential Treatments for Cancer, Alzheimer’s, Journal Claims – TIME

“Potential treatments for Alzheimer’s disease, cancer and many other illnesses are being blocked by anti-drug laws, according to a new editorial review published in Nature Reviews Neuroscience.”

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Large Study Finds No Link between Marijuana and Lung Cancer – Scientific American

“…Scientists were therefore surprised to learn that a study of more than 2,000 people found no increase in the risk of developing lung cancer for marijuana smokers.

“We expected that we would find that a history of heavy marijuana use–more than 500 to 1,000 uses–would increase the risk of cancer from several years to decades after exposure to marijuana,” explains physician Donald Tashkin of the University of California, Los Angeles, and lead researcher on the project. But looking at residents of Los Angeles County, the scientists found that even those who smoked more than 20,000 joints in their life did not have an increased risk of lung cancer.

The study does not reveal how marijuana avoids causing cancer. Tashkin speculates that perhaps the THC chemical in marijuana smoke prompts aging cells to die before becoming cancerous. Tashkin and his colleagues presented the findings yesterday at a meeting of the American Thoracic Society in San Diego.”

More: http://www.scientificamerican.com/article.cfm?id=large-study-finds-no-link

Marijuana Smoking Not Linked To Cancer or Lung Damage, Researchers Say

 “Donald Tashkin’s is a tale cannabis pushers like to repeat. The physician and professor at UCLA’s David Geffen School of Medicine set out to prove — via a study funded by the National Institutes on Drug Abuse — that marijuana is bad for you. Instead, a long-term study found no solid link between marijuana use and lung cancer, in sharp contrast to tobacco terrible effects on health.” 

donald-tashkin.jpg

“Similar findings were repeated all over the world. In a collection and review of studies on marijuana’s effect on the lungs, published in the June issue of the Annals of the American Thoracic Society, Tashkin concludes that compared to tobacco smoking, heavy marijuana use has “relatively small and far lower” risks.

This despite an average joint marijuana having four times the tar of a typical American Spirit. How can this be?

It’s worth remembering that this is not a new development — Tashkin’s long-term study was published in 2006. And well before that — as in the 19th Century, when cannabis tinctures and other marijuana medicines were sold in pharmacies — doctors were prescribing marijuana as a treatment for asthma patients.”

More: http://blogs.sfweekly.com/thesnitch/2013/06/marijuana_cancer_annals_of_the_american_thoracic_society.php

Breathe Easy: A Marijuana Study Finds No Lung Cancer Links

Donald Tashkin‘s is a tale cannabis pushers like to repeat. The physician and professor at UCLA‘s David Geffen School of Medicine set out to prove — via a study funded by the National Institutes on Drug Abuse — that marijuana is bad for you. Instead, a long-term study found no solid link between marijuana use and lung cancer.

Similar findings were repeated all over the world. In a review of studies on marijuana’s effect on the lungs, published in the June issue of the Annals of the American Thoracic Society, Tashkin concludes that compared to tobacco smoking, heavy marijuana use has “relatively small and far lower” risks.”

More: http://www.sfweekly.com/2013-06-19/news/ucla-medical-marijuana-cancer/full/