Long-Term Effects of Alcohol on the Intestines
The biological mechanisms mediating alcohol-related cancer are not fully understood, although it is known alcoholic beverages contain at least 15 carcinogenic compounds. These include acetaldehyde, acrylamide, aflatoxins, arsenic, benzene, cadmium, ethanol, ethyl carbamate, formaldehyde and lead, with ethanol being the most important carcinogen. The foremost toxic product of alcohol metabolism is acetaldehyde, which forms through an oxidative process and also occurs naturally in alcoholic beverages. Acetaldehyde produces carcinogenic and genotoxic effects when it comes in contact with the upper aerodigestive tract (pharynx, oral cavity, esophagus and larynx). Alcohol first contacts the oral cavity, followed by the esophagus, therefore oral and esophageal cancers present the highest relative risks of alcohol-related cancer. In esophageal cancer, it does not appear to matter if a person drinks wine, beer or spirits, although hard liquor more easily destroys the fine protective layer on the esophagus.3
In a meta-analysis of 222 studies comprising 92,000 light drinkers and 60,000 nondrinkers with cancer, light drinking was associated with a high risk of esophageal squamous cell carcinoma. This analysis showed an estimated 24,000 deaths from esophageal squamous cell carcinoma were attributable to light drinking. One has to keep in mind when alcohol use is self-reported, individuals may underestimate or underreport actual alcohol intake, which could mean higher drinking levels contributed to these cancer deaths.3
Esophageal Variceal Hemorrhage
Esophageal varices (distended veins) impact the lower esophagus or the upper part of the stomach. This type of varices is particularly dangerous because increased pressure within the vein can cause them to burst, leading to a critical loss of blood. In people with alcohol- or obesity-related liver cirrhosis, varices can develop when blood flow through the liver is obstructed by scarring. The varices increase the pressure inside the portal vein, which carries blood from the intestines to the liver, a condition called portal hypertension.4
Esophageal variceal hemorrhage is a life-threatening complication of portal hypertension associated with a much higher death rate than other causes of GI bleeding. Clinical factors associated with an increased risk of variceal bleeding include poor liver function and ongoing alcohol abuse. Some reports indicate variceal bleeding accounts for 11% to 20% of all upper GI bleeding, while 12 to 14 other studies suggest they are responsible for 50% to 80% of GI bleeding episodes.5 The estimated mortality rate for the first episode of variceal hemorrhage is 30% to 50%, which is dependent on the severity of the underlying liver disease. Individuals who experience one episode of bleeding from esophageal varices have a 60% to 80% chance of re-bleeding within one year of the initial episode. Approximately one-third of recurrent bleeding episodes are fatal.6
A retrospective study analyzed 45 sudden fatal death cases (28 men and 17 women) involving esophageal variceal hemorrhage outside the hospital setting. All of the deceased were white, with an age range of 24 to 72 (average age 50.6 years). Ruptured esophageal varices were located in the lower third of the esophagus in 44 cases. Cirrhosis of the liver was present in all cases, of which 42 were alcohol-related based on a known history of chronic alcohol consumption. A hepatocellular carcinoma was found in three cases. Alcohol-induced pancreatic tissue alterations were frequently found and 30 toxicology reports were positive for alcohol in blood and urine samples. Of the 45 cases, 37 deaths were attributed to esophageal variceal rupture alone. The remaining eight deaths were attributed to a combination of severe loss of blood and the following coexisting diseases: five cases of decompensated diabetes and one each of bronchopneumonia, dilated cardiomyopathy and acute hemorrhagic pancreatitis.5
Gastrointestinal bleeding (GIB) is a common and potentially life threatening medical problem accounting for more than 200,000 inpatient admissions and 7,000 deaths in the U.S., annually. Most studies of non-variceal bleeding have focused on peptic ulcers, with conflicting findings linking bleeding to alcohol consumption. A large-scale study involving men indicated the risk of GIB increased with the amount of liquor consumed. After adjusting for other potential risk factors, individuals who consumed five or more alcoholic drinks per week had an increased risk of GIB compared to those who consumed liquor less than once per month. The major finding was upper GIB secondary to peptic ulcer disease. The risk of GIB was also higher among men who consumed alcohol without meals compared to those who drank with meals. Alcohol consumption coupled with regular use of nonsteroidal anti-inflammatory drugs (NSAIDs) and/or aspirin potentiated the risk of GIB. In general, men who consumed more alcohol were more likely to be a current or past smoker and be regular users of aspirin or NSAIDs. Neither past nor current smoking appeared to have a significant effect on GIB risk.7
In the last decade, the decreasing prevalence of Helicobacter pylori (H. pylori) infection and improvement of peptic ulcer treatment such as proton pump inhibitors has reduced the incidence of uncomplicated peptic ulcer disease. In the same timeframe, however, several studies have shown controversial results showing unchanged incidence of complicated peptic ulcer disease, likely due to multifactorial risk factors. Limited studies have examined the association between aging or alcohol consumption and complicated peptic ulcer disease. A Korean study involving 396 individuals (average age 50.6) diagnosed with perforated peptic ulcer (PPU) revealed 47% consumed alcohol (more than 20 g of alcohol a week) and 55.8% had a smoking habit. Older age and alcohol consumption were significant risk factors for PPU not associated with H. pylori or NSAIDs.8
Gastritis is a largely preventable and treatable disease, which results in inflammation of the lining of the stomach. Acute gastritis may present with an array of symptoms, the most common being nondescript abdominal discomfort. Additional symptoms include nausea, vomiting, loss of appetite, belching and bloating. Alcohol is an irritant that induces inflammatory changes in the gastric mucosa. Evidence of H. pylori infection is found in 20% of individuals younger than 40 and 50% of individuals older than 60. Alcoholic gastritis is most associated with hard liquor such as whisky, vodka and gin. Complications of acute gastritis include bleeding from an erosion or ulcer, gastric outlet obstruction, dehydration from vomiting and renal insufficiency as a result of dehydration.9
Gastroesophageal reflux disease, commonly referred to as GERD, is one of the most common disorders, with an increasing incidence and prevalence over the last two decades. Alcohol consumption may increase symptoms of GERD and cause damage to the esophageal mucosa. Individuals with symptomatic GERD are often advised to avoid alcohol consumption or to consume moderate amounts of alcohol to help alleviate symptoms. The scientific evidence linking GERD to more general alcohol consumption has been inconsistent. Although the association has not been fully elucidated, it is hypothesized multiple factors may contribute to the potential GERD/alcohol connection, including esophageal and gastric muscosal damage, some of which may be attributed to the toxic effects of metabolized acetaldehyde.10
Gastric cancer, also known as stomach cancer, is one of the most prevalent cancers, although worldwide morbidity and mortality rates have declined rapidly over the past few decades. The American Cancer Society estimated 28,000 people in the U.S. will be diagnosed with stomach cancer in 2017 and about 10,960 will die from the disease.11 The relationship between alcoholic beverages and gastric cancer is biologically plausible because ethanol is fat soluble and can damage the gastric mucosa. Moreover, acetaldehyde can have a local toxic effect, which could be a potential contributing factor in the development of gastric cancer. A meta-analytic study investigated the alcohol-gastric cancer connection including comparative risk in moderate and heavy drinkers and dose-dependent risk. The analysis of 10 studies confirmed that alcohol consumption can increase the risk of gastric cancer even at lower levels of consumption.12
A meta-analysis of 57 cohort and case-control studies examined the association between alcohol consumption and colorectal cancer risk. The study showed people who regularly drank 50 or more grams of alcohol per day (approximately 3.5 drinks) had a 1.5 increased risk of developing colorectal cancer as nondrinkers or occasional drinkers. For every 10 grams of alcohol consumed per day, there was a 7% increase in the risk of colorectal cancer.13
Diarrhea and Vomiting
Diarrhea and vomiting are two of the classic symptoms of a hangover, but they can also be associated with the earliest stage of alcohol withdrawal or alcohol-related inflammation of the GI tract. Alcohol can cause the stomach to produce more acid than normal, inhibit absorption of water from the large intestine, decrease digestive enzymes and speed up the passage of stools, all of which can result in diarrhea.14 Vomiting can be a sign of alcohol poisoning, excessive drinking, hangover or occur during alcohol withdrawal.
Clearly, alcohol wreaks havoc on every part of the body including the digestive system. Although chronic alcohol consumption may have already wreaked damage on your body, it’s not too late to seek treatment and stop drinking.
- Alcohol's Effects on the Body. National Institute on Alcohol Abuse and Alcoholism website. https://www.niaaa.nih.gov/alcohol-health/alcohols-effects-body Accessed May 26, 2017.
- Gastrointestinal Tract (GI Tract). PubMed Health website. https://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0022855/ Accessed May 26, 2017.
- No Amount of Alcohol Is Safe. Medscape website. http://www.medscape.com/viewarticle/824237 Published April 30, 2014. Accessed May 26, 2017.
- Patient education: Esophageal varices (Beyond the Basics). UptoDate website. https://www.uptodate.com/contents/esophageal-varices-beyond-the-basics Updated August 10, 2016. Accessed May 26, 2017.
- Tsokos M, Türk EE. Esophageal Variceal Hemorrhage Presenting as Sudden Death in Outpatients. Arch Pathol Lab Med. 2002 Oct;126(10):1197-200.
- Portal Hypertension. Medscape website. http://emedicine.medscape.com/article/182098-overview#a7 Published November 20, 2016. Accessed May 26, 2017.
- Strate LL, Singh P, Boylan MR, Piawah S, Cao Y, Chan AT. A Prospective Study of Alcohol Consumption and Smoking and the Risk of Major Gastrointestinal Bleeding in Men. Green J, ed. PLoS ONE. 2016;11(11):e0165278. doi:10.1371/journal.pone.0165278.
- Yang YJ, Bang CS, Shin SP, et al. Clinical characteristics of peptic ulcer perforation in Korea. World J Gastroenterol. 2017;23(14):2566-2574. doi:10.3748/wjg.v23.i14.2566.
- Acute Gastritis. Medscape website. http://emedicine.medscape.com/article/175909-overview Published February 25, 2016. Accessed May 26, 2017.
- Chen S, Wang J, Li Y. Is alcohol consumption associated with gastroesophageal reflux disease? J Zhejiang Univ Sci B. 2010;11(6):423-428. doi:10.1631/jzus.B1000013.
- What Are the Key Statistics About Stomach Cancer? American Cancer Society website. https://www.cancer.org/cancer/stomach-cancer/about/key-statistics.html Updated January 6, 2017. Accessed May 26, 2017.
- Ma K, Baloch Z, He T-T, Xia X. Alcohol Consumption and Gastric Cancer Risk: A Meta-Analysis. Med Sci Monit. 2017;23:238-246. doi:10.12659/MSM.899423.
- Alcohol and Cancer Risk. National Cancer Institute website. https://www.cancer.gov/about-cancer/causes-prevention/risk/alcohol/alcohol-fact-sheet Published June 24, 2013. Accessed May 26, 2017.
- Diarrhea After Drinking – Causes and Treatment. Diarrhea Nurse website. http://www.diarrheanurse.com/diarrhea-after-drinking.html Accessed May 26, 2017.