The Healthcare Professional's

Core Resource on Alcohol

Knowledge. Impacts. Strategies.

Medical Complications: Common Alcohol-Related Concerns

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    Takeaways

    • Alcohol is a leading cause of morbidity and mortality, with harms related to both acute and chronic effects of alcohol contributing to about 5 million emergency department visits and more than 178,000 deaths in the U.S. each year.
    • There is no perfectly safe level of alcohol consumption, as current research points to health risks including cancer and cardiovascular risks even at low levels of consumption, regardless of beverage type.
    • Alcohol is a carcinogen associated with cancer of the oral cavity, pharynx, larynx, esophagus, colon, rectum, liver, and female breast, with breast cancer risk rising with less than one drink a day.
    • Many organs and body systems are impacted by alcohol use—not just the liver, but also the brain, gut, pancreas, lungs, cardiovascular system, immune system, and more—which can explain, for example, challenges in managing hypertension, atrial fibrillation, diabetes, and recurrent lung infections.
    • Your patients may be unaware that their alcohol use may be contributing to their medical problems and risks. During brief interventions, you can help patients to see that they can

    Alcohol’s harmful effects on multiple organs and body systems contribute to more than 200 health conditions and more than 178,000 deaths in the U.S. each year, making alcohol one of the leading causes of preventable death.1–4 More than half of the deaths result from chronic heavy alcohol consumption while the remainder result from acute injuries sustained while intoxicated. 5

    The health risks of alcohol tend to be dose-dependent, and the likelihood of certain harms, such as cancer, begin at relatively low amounts.6 Even drinking within the U.S. Dietary Guidelines (see drinking level terms below), for example, increases the risk of breast cancer.7,8 Additionally, earlier research suggested cardiovascular benefits, but newer, more rigorous studies are finding little or no protective effect of alcohol on cardiovascular or other outcomes.9–13 In short, current research indicates there is no safe drinking level,9 underscoring the message to patients that “the less, the better” when it comes to alcohol.

    A note on drinking level terms used in this Core article: The 2020-2025 U.S. Dietary Guidelines states that for adults who choose to drink alcohol, women should have 1 drink or less in a day and men should have 2 drinks or less in a day. These amounts are not intended as an average but rather a daily limit. Binge drinking is a drinking pattern that brings a person’s blood alcohol concentration to 0.08 percent or more, which typically happens if a woman has 4 or more drinks, or a man has 5 or more drinks, within about 2 hours. Heavy drinking includes binge drinking and has been defined for women as 4 or more drinks on any day or 8 or more per week, and for men as 5 or more drinks on any day or 15 or more per week.

    Here, we provide a brief overview of common medical problems that may be related to your patients’ consumption of alcohol.

    Medical complications by body system

    Below are potential alcohol-related medical complications by body system.

    Gastrointestinal system

    Several prominent complications of heavy alcohol use involve the gastrointestinal (GI) system.

    Liver disease: Because 90% of absorbed alcohol is metabolized in the liver, this organ is extensively exposed not only to alcohol but also to toxic alcohol metabolites and is vulnerable to severe acute and chronic injury. Alcohol-associated liver disease (ALD) plays a major and growing role in alcohol-related morbidity and mortality in the U.S.

    • ALD includes a pathological spectrum of alcohol-related liver injury. Drinking beyond U.S. Dietary Guidelines levels can cause liver disease, including steatosis (accumulation of fat), steatohepatitis (inflammation), fibrosis and cirrhosis (scarring), hepatocellular carcinoma, and alcohol-associated hepatitis. The stages of ALD are not necessarily progressive, and multiple stages can be present in one individual with long-standing heavy drinking.Factors that promote the progression from steatosis to advanced ALD include continued heavy drinking; being female, older age, or obese; smoking; and having viral 14
      • Steatosis, or fatty liver, is the earliest sign of liver injury and is present in about 95-100% of people who drink heavily.15 Lipid accumulation in hepatocytes and increased liver size are hallmarks of steatosis. Steatosis is fully reversible if alcohol consumption stops. However, 10-35% of people with steatosis who continue to drink develop inflammation and progress to a more advanced stage of liver injury, steatohepatitis.15
      • Steatohepatitis is defined by the presence of fatty liver, lobular inflammation, and hepatocellular damage in the form of hepatocellular ballooning—all in various degrees of severity. In a subset of patients, chronic steatohepatitis may slowly progress to fibrosis (in 20–40% of patients) and cirrhosis (in 8–20% of patients).16
      • Fibrosis and cirrhosis in ALD involve collagen deposits that form a “chicken wire” pattern, typically around the terminal hepatic vein and along the sinusoids. Advanced fibrosis severely impairs hepatic architecture and blood flow, characteristics of the cirrhotic stage. Portal hypertension, hepatic encephalopathy, and hepatorenal syndrome are well known, life-threatening complications of alcohol-associated cirrhosis. The liver generally does not heal from cirrhosis and transplants often are needed. In addition, about 2% of patients with cirrhosis develop primary hepatocellular carcinoma.17
      • Alcohol-associated hepatitis (AH) is a clinical syndrome that develops suddenly in approximately 20% of people who drink heavily.18,19 AH is characterized by a rapid onset of jaundice, liver synthetic dysfunction, and hepatic decompensation. An episode of AH is frequently the first clinical presentation of ALD. In patients with severe AH, the prognosis is poor; mortality is 20-40% at 3 months overall and up to 70% in patients who don’t respond to corticosteroids.20 AH can occur in any stage of liver disease, and up to 80% of patients with severe AH may have underlying cirrhosis.21
    • Severe ALD morbidity as well as mortality are on the rise. The proportion of ALD patients who progress to cirrhosis and other forms of severe disorder requiring hospitalizations and transplants has increased markedly in the U.S. since the early 2000s.22 For example, the number of ALD patients listed for liver transplant increased by 63% from 2007 to 2017, 22 and ALD is now the leading reason for liver transplantation in the country.23,24 Liver cirrhosis caused about 48,000 deaths nationwide in 2019, half of which were alcohol-related.25 The death rate for alcohol-related cirrhosis increased by 47% between 2000 and 2019, from 4.3 to 6.4 deaths per 100,000 population.25
    • Abstinence is needed to improve the prognosis for ALD.16,26 Patients at any stage of ALD who have alcohol use disorder (AUD) should receive AUD treatment and be urged to maintain abstinence.27,28 (See Core article on treatment.) In cases of steatosis, abstinence can allow the liver to heal. In cases of cirrhosis, abstinence helps prevent further liver damage and increases the survival rate significantly compared to patients who return to drinking alcohol.29

    The rising rates of severe morbidity and mortality from ALD underscore a pressing need to screen patients for heavy drinking, assess for AUD, and recommend evidence-based AUD treatment. (See Core articles on screening and assessment and treatment. For practice guidance on diagnosing and treating ALD, see Resources below).

    Pancreatitis: Alcohol is the leading cause of chronic pancreatitis and the second leading cause of acute pancreatitis after gallstones.30 Acute pancreatitis is a top reason for GI-related hospitalization in the U.S., with about 291,000 admissions annually. 31 Up to 20% of these cases have serious complications that carry a mortality rate of up to 30%.32 Acute pancreatitis equally affects both men and women, whereas chronic pancreatitis is more common in men.33 Smoking independently raises the risk for both types of pancreatitis and could synergize the effects of alcohol.34

    GI inflammation and bleeding: Among its effects on the GI system, alcohol can damage the epithelial lining of the GI tract, promote inflammation within and beyond the GI system, and cause GI bleeding.

    • GI inflammation: Alcohol can damage the mucous membranes lining the esophagus, stomach, and intestinal tract, leading to inflammation.35–37 One night of binge drinking can inflame the intestines and impair intestinal barrier function, allowing toxins from gut-inhabiting bacteria to enter the systemic circulation.38,39 Over time, the inflammatory response triggered by these compounds contributes to damage to the liver, brain, and potentially other organs.39,40
    • GI bleeding: Alcohol can damage the mucosa severely enough to cause GI bleeds. A longitudinal study of men found that those who drank more than two drinks per day were 43% more likely to develop major GI bleeds compared with those who did not drink.41 Alcohol also enhanced the risk of GI bleeds associated with aspirin or other NSAIDs. 41 Another study found that 1 in 5 patients hospitalized for GI bleeds drank heavily.42 Furthermore, people who drink heavily were nearly twice as likely to have repeated bleeds over the following 6 months and were 50% more likely to die over the following 5 years.42

    Gastroesophageal reflux disease (GERD): Alcohol consumption is associated with an increased risk of GERD, with the level of risk increasing with both drinking volume and frequency.43 Drinking about one serving of alcohol per day is associated with a 16% increase in the risk of developing GERD.43

    Immune system

    Both acute and chronic heavy use of alcohol can interfere with multiple aspects of the immune response,44–46 the result of which can impair the body’s defense against infection, impede recovery from tissue injury, cause inflammation, and contribute to alcohol-related organ damage.47

    • Immune signaling, infection defense, and wound healing: Both a single episode of binge drinking and long-term heavy drinking can alter cytokine and chemokine signaling between immune cells involved in coordinating an immune response to injury or infection,48–51 and thus may reduce the ability of the innate immune system to fight infections.38 Chronic alcohol exposure causes impaired wound healing and may increase the incidence of wound infection.52
    • Inflammation: Damage to the gut epithelium from heavy alcohol use can allow microbial particles to leak into circulation and cause inflammation in the liver, brain, and body as a whole.35,53 Chronic alcohol consumption increases levels of circulating pro-inflammatory cytokines, potentially adding to inflammation caused by disease or natural aging.54,55 Chronic heavy alcohol consumption can damage the integrity of the epithelial barrier in the lungs, causing inflammation and increasing the risk of both infection and Acute Respiratory Distress Syndrome (see next section).56,57

    For more on this topic, see the NIAAA journal issue on Alcohol and the Immune System.58

    In addition to these biological influences of alcohol on the immune system, drinking can contribute to the spread of disease, such as HIV and possibly COVID-19, by facilitating risky behaviors.59

    Endocrine system

    Heavy alcohol use has the potential to disrupt the endocrine system’s many chemical pathways that normally help maintain homeostasis and health.60

    • The endocrine system: Heavy alcohol use can cause disturbances across all components of the endocrine system, including, for example, peripheral endocrine glands controlled by the hypothalamic-pituitary axis (such as the thyroid, adrenal glands, and gonads) as well as the endocrine components of organs such as the pancreas and adipose tissue.60 Heavy drinking not only causes hormonal disturbances within the endocrine system, but also disrupts the release of neurotransmitters and cytokines involved in the crosstalk between the endocrine, nervous, and immune systems. Because these disturbances permeate every organ and tissue in the body, they can contribute to endocrine-related health conditions including diabetes (see next bullet), thyroid diseases, dyslipidemia, and reproductive dysfunction.60 For more information, see the NIAAA journal article on the effects of alcohol on the endocrine system.
    • Diabetes: In patients with diabetes, any alcohol intake may reduce their ability to control blood glucose levels adequately61–63 and thus contributes to the progression of diabetes-associated cardiovascular and neurologic complications.62,64,65 Furthermore, heavy drinking may increase the risk for developing Type 2 diabetes via several mechanisms, including increased body weight, blood triglyceride levels, or blood pressure, and decreased insulin sensitivity4 —all known risk factors for diabetes.

    Pulmonary system

    Alcohol impairs ciliary function in the upper airways, disrupts the function of immune cells (i.e., alveolar macrophages and neutrophils), and weakens the barrier function of the epithelia in the lower airways.44 Often, alcohol-provoked lung damage goes undetected until a second insult, such as a respiratory infection, leads to more severe lung diseases than those seen in nondrinkers.47

    • Pneumonia: There is a strong dose-response association between alcohol use and community-acquired pneumonia, with the relative risk of pneumonia rising 6-8% per drink per day, independent of smoking.66 When hospitalized with pneumonia, patients with alcohol-related problems, particularly those in withdrawal, are at increased risk of poor outcomes.67,68
    • Acute Respiratory Distress Syndrome (ARDS): Long-term heavy drinking raises the risk for respiratory infections and for ARDS,69 with increased need for mechanical ventilation, prolonged stay in the intensive care unit, and greater mortality.70–72 Alcohol-related harm to the epithelial barrier and impaired macrophage function in the lung may underlie increased rates of ARDS in patients with heavy alcohol use.69,73
    • Pulmonary consequences of COVID 19: It will take time for research to assess how alcohol may affect the risk and severity of COVID-19. As noted above, long-term heavy drinking raises the risk for respiratory infections and for ARDS. Patients with more severe COVID-19 often develop ARDS,74 and in these cases, the effects of heavy drinking on the immune system may exacerbate the ARDS and worsen the prognosis. 

    Cardiovascular system

    Alcohol consumption can negatively impact the cardiovascular system in a variety of ways. Heavy alcohol use causes 9,000 deaths per year from heart disease and stroke,75 and even low levels of use are associated with increased risk for hypertension,76 arrythmias,77 heart attack,78 and stroke.78 Current research indicates that overall, even when it comes to heart disease, the less alcohol, the better.79

    • Blood pressure: Heavy alcohol consumption is linked with elevated systolic and diastolic blood pressure,80 and among people who drink heavily, reducing alcohol intake lowers blood pressure in a dose-dependent manner.81 Even at low levels of intake (1 to 2 drinks per day), alcohol is associated with an increased risk of hypertension for men, with research indicating a 19% risk increase, compared with men who do not drink.76 For women, hypertension risk increases at drinking levels beyond 1 to 2 drinks a day.76
    • Arrythmia: Both acute and chronic alcohol use are associated with arrythmias, even in people with no clinical history of atrial fibrillation (AF) or structural disease.82 Even less than one drink per day is associated with an increased risk of developing AF.77 Heavy alcohol intake, even one binge drinking episode, can alter the heart’s electrophysiology, leading, for example, to an acute arrhythmia known as “holiday heart syndrome.”82 Moreover, chronic heavy alcohol consumption is associated with an increased likelihood of developing AF over time.83 In patients with a history of AF, reducing alcohol consumption to near-abstinence levels may lower the risk of recurrence of AF,84 although some research indicates that any alcohol use raises the risk for an AF episode in the hours that follow consumption.85
    • Cardiomyopathy: Chronic heavy alcohol consumption can cause cardiomyopathy leading to progressive reduction in heart muscle contractility and heart chamber dilation.86–89 Abstinence or reductions in consumption are associated with improvements in heart health in patients with cardiomyopathy.90
    • Myocardial infarction: Chronic, heavy drinking raises the risk for ischemic heart disease,6,9 and even low drinking levels may confer risk.10,11 Beginning with just 1 to 2 drinks, there is an increased risk of heart attack immediately after alcohol consumption, which diminishes over the next 24 hours.78 With heavier intake, however, the risk continues into the following week.78 Although earlier research linked low levels of alcohol consumption with a reduced risk of ischemic disease,6,9 the latest and most rigorous research indicates that cardiovascular benefits have been overestimated.79,91 Earlier study methods made it difficult to conclude whether positive cardiovascular outcomes were due to low alcohol consumption or instead to differences in factors such as genetics, health history, and diet and other health behaviors. One source of bias in older studies, for example, was having control groups comprised of non-drinkers, many of whom did not drink due to illness. Newer studies that use light drinkers as the control group and take into consideration differences in health-related behaviors of lighter drinkers do not find the robust protective effects of alcohol noted in prior studies. 9,12
    • Stroke: The risk for ischemic and hemorrhagic stroke increases not only with chronic, heavy drinking6,9 but also with low levels of consumption, 10,11 and may increase by as much as 14% with just one drink per day on average.10 As with myocardial infarction, the risk of stroke increases immediately after consuming just 1 to 2 drinks, and diminishes over the next 24 hours.78

    Hematological system

    Heavy alcohol use can cause anemia, leukopenia, and thrombocytopenia as well as macrocytosis. It is unclear to what extent these abnormalities are caused directly by marrow toxicity or indirectly by liver disease, hypersplenism, and nutritional deficiencies.92,93

    Musculoskeletal system

    Heavy alcohol use raises the risk for myopathies and fractures, whereas even low levels of alcohol intake increase the odds for recurrent gout attacks.

    • Skeletal muscle myopathy: Chronic, heavy alcohol intake causes a chronic myopathy marked by progressive midline muscle weakness and atrophy. 94,95 These chronic alcohol-related myopathies affect approximately 50% of patients with AUD,96 and occur far more frequently than inherited myopathies. In contrast, acute alcohol-related myopathies affect approximately 1-2% of patients with AUD, 96,97 and can occur following a single severe binge drinking episode. 96,97
    • Fracture: Drinking more than about 1.5 to 2 drinks a day is associated with an increased risk of hip and other types of fractures, including osteoporotic fractures.98,99 Alcohol can disrupt the balance between the erosion and remodeling of bone tissue, contributing to decreased bone density and increased risk of fracture.100 Among those who drink heavily, it is likely that falls contribute to the increased fracture risk.99 Even people who drink less than heavily are significantly more likely to be injured in falls than people who do not drink.101
    • Gout: The risk of developing gout increases in a dose-dependent fashion with alcohol intake, with relative risks of 1.6 for those who drink 1 to 2 drinks per day and 2.6 for those who drink 3 or more drinks per day, compared with non-drinkers or those who drink only occasionally.102 Moreover, evidence shows that the risk of recurrent gout attacks rises with the level of alcohol consumed, starting with a 36% higher risk with just 1 to 2 drinks in a single day.103 Although often associated only with drinking beer or distilled spirits, research indicates that consuming any type of alcohol—beer, wine, or spirits—increases gout attack risk.103

    Neurologic system

    Severe AUD is associated with damage to the central nervous system and peripheral nerves.

    • Central nervous system: Research links heavy alcohol use and moderate to severe AUD with damage to both white and gray matter in the brain, as well as deficits in cognitive functions.104 Heavy drinking can alter the trajectory of adolescent brain development105–107 and contributes to dementia in older drinkers.104,108–112 Heavy alcohol use over time damages the brain through a combination of direct neurotoxic effects, nutritional deficiencies, neuroinflammation, liver disease, and metabolic abnormalities,109,113 all exacerbated by aging.114 Alcohol neurotoxicity reduces synaptic complexity, 110,111 alters communication between nerve cells, 110,111 and decreases brain volume,112 particularly in frontal regions.104,109 Brain damage due to alcohol can manifest in problems with attention, memory, and reasoning.104 Abstinence may partially reverse these changes.115 For an introduction to the brain regions and neurocircuits involved in AUD, see the Core neuroscience
    • Peripheral nervous system: Peripheral neuropathy occurs commonly in severe AUD. The underlying cause is alcohol neurotoxicity, sometimes heightened by nutritional deficiency.116–118 Alcohol-induced peripheral neuropathy causes a symmetrical “stocking-glove” sensory loss in the extremities and often painful burning in the feet. These neuropathies are distinct from incidents of localized, acute nerve compression resulting from prolonged immobilization due to alcohol intoxication. Alcohol-related damage to autonomic nerves may also cause cardiac arrythmias, postural hypotension, diarrhea, and erectile dysfunction.119,120 Abstinence may lead to improvement of symptoms.121
    • Wernicke’s encephalopathy: Severe AUD can result in reduced food intake and malabsorption of thiamine, which leads to thiamine deficiency.122 In turn, thiamine deficiency can cause Wernicke’s encephalopathy (WE).123,124 Often underdiagnosed, WE is a treatable neurologic emergency affecting both the central and peripheral nervous systems.125 Any symptoms of WE in patients with AUD—such as mental confusion, vision problems, gait coordination problems, hypothermia, low blood pressure, lethargy, or coma126—should prompt immediate high-dose thiamine treatment.127,128 Treatment of WE within hours of the development of symptoms is critical, as a delay is likely to result in death or permanent neurological disabilities, including Korsakoff syndrome,129–131 which is marked by irreversible memory impairments (see next bullet).
    • Korsakoff syndrome: When untreated or undertreated, WE can progress to Korsakoff ’s syndrome (KS), characterized by profound amnesia and frequently accompanied by gait abnormalities and false memories. The precise neuropathology responsible for these symptoms has not been fully determined, but the profound amnesia in KS is thought to result from damage along the hippocampal-anterior thalamic axis.128,132,133 A majority of patients with KS require prolonged institutional care.134 Some degree of recovery may occur over many months and is dependent on treatment of nutritional deficiencies and abstinence from alcohol.115,135,136 Studies have not demonstrated a beneficial effect from pharmacological therapy, but memory rehabilitation programs have shown promising results.137,138

    Complications affecting multiple body systems

    Examples of alcohol-related complications that can affect multiple body systems are described below.

    Acute harm and medical emergencies

    Acute alcohol-related injuries and death can be the consequence of a single binge-drinking episode or long-term heavy drinking. The rate of emergency department visits related to acute and chronic alcohol use increased 47.0% between 2006 and 2014, which translates to an average increase of 210,000 alcohol-related visits per year.139 Among the risks:

    • A single binge-drinking episode significantly increases the likelihood of motor vehicle crashes,140 drownings,141 hypothermia,142,143 trauma in general,144–146 higher risk sexual behaviors and infections,147–151 falls, burns, and suicides,152,153 and overdoses from alcohol on its own or by potentiating overdose risk from other sedating drugs (see Core article on medication interactions).152,153
    • Heavy drinking over a long period of time can lead to emergency medical visits for potentially life-threatening withdrawal symptoms as well as complications of chronic alcohol-related problems139 including liver disease, pancreatitis, GI bleeding, and many other conditions listed above. Alcohol withdrawal accounts for approximately 260,000 emergency department visits154 and 850 deaths155 in the U.S. each year. For details about alcohol withdrawal, see the Core article on AUD.

    Screening and brief interventions for heavy alcohol use conducted in EDs show promise for reducing alcohol consumption after discharge.139 (See Core articles on screening and brief intervention.)

    Alcohol exposure during pregnancy: Risk of fetal alcohol spectrum disorders

    Prenatal alcohol exposure can cause lifelong physical, behavioral, and cognitive impairments collectively known as fetal alcohol spectrum disorders (FASD), a leading cause of preventable intellectual disability and birth defects in the U.S. 156,157 Awareness of the potential harms of prenatal alcohol exposure may be limited, however, among both the general public and clinicians. A brief overview follows.

    • No amount of alcohol known to be safe in any trimester: Alcohol can have harmful effects throughout gestation, with binge drinking thought to be particularly damaging.156,158,159Even lower levels of alcohol exposure during pregnancy are associated with increased risks for miscarriage,160 and for adverse behavioral and psychological outcomes in children.161 And the risk for Sudden Infant Death Syndrome (SIDS) is elevated with continued drinking beyond the first trimester.162
    • Advice to abstain during pregnancy: Obstetric and pediatric guidelines advise maternal abstinence throughout pregnancy.156,163,164 Moreover, the U.S. Surgeon General recommends that women who are considering becoming pregnant abstain from alcohol.165
    • Multiple disorders: FASD encompasses a range of possible disorders based on the type and degree of impairments.156,157,163 These developmental disorders include: 166,167
    • Estimated prevalence of prenatal alcohol exposure and FASD: About 1 in 9 pregnant women report drinking in the U.S., and among them, almost half report binge drinking.168 There has been a slightly increasing trend from 2011 to 2020 in current and binge drinking during pregnancy.169 An estimated 1-5% of first-grade children have FASD, which is comparable to or even more common than the prevalence of autism spectrum disorder.157,170
    • Damage to the brain: Alcohol exposure can alter prenatal brain development, structure, and activity, resulting in lifelong cognitive, social, and behavioral deficits as well as motor and coordination problems.171 Milder forms of FASD may cause subtle neurodevelopmental effects that do not prompt clinical attention.157 In part because only a minority of individuals with FASD have facial dysmorphology, central nervous system deficits may be attributed to other conditions, and FASD remains under-diagnosed.157
    • Multiple challenges from primary and secondary disabilities: Each individual with FASD experiences a unique combination of day-to-day challenges caused not only by the primary cognitive and behavioral disabilities associated with FASD, but also by secondary disabilities involving medical, mental health, educational, and social issues that may be even more challenging.172 With early identification and intervention, some disabilities may be mitigated, but health system improvements are greatly needed to increase awareness of FASD and access to diagnostic and intervention services.173

    See the Resources section, below, for guidance and training opportunities for healthcare professionals on FASD prevention, diagnosis, and early interventions from the American College of Obstetricians, the American Academy of Pediatrics, the Association of Maternal and Child Health Programs, and the Centers for Disease Control and Prevention. For additional information, see the NIAAA fact sheet on FASD.

    Cancer

    Alcohol and its metabolite acetaldehyde are carcinogens linked with an increased risk for numerous cancers in humans, 174–177 and accounted for an estimated 5.6% of cancer cases and 4% of cancer deaths in the U.S. according to a 2017 analysis.178 Fewer than half of Americans, however, recognize that alcohol is a risk factor for cancer. 179

    • Confirmed alcohol-cancer associations: Studies show dose-response associations between alcohol consumption and cancers of the oral cavity, pharynx, larynx, esophagus, colon, rectum, liver, and female breast.174 The harm appears to be independent of type of alcohol (beer, wine, liquor).175,176
      • Breast cancer: Even less than 1 drink per day is associated with a roughly 10% increase in breast cancer risk.7,180 An estimated 39,000 female breast cancer cases in the U.S. annually, or about 16% of U.S. cases, are attributable to alcohol use.178
      • Esophageal and head and neck cancers: These cancers have the highest relative risk, such that people who drink heavily have five times the risk of developing these cancers compared to people who drink only occasionally or not at all.181
      • Esophageal cancer risk in East Asian populations: An estimated 36% of people of East Asian descent (Chinese, Japanese, and Korean heritage) carry gene variants that disrupt the functioning of key enzymes involved in alcohol metabolism, such as aldehyde dehydrogenase (see Core article on the basics).182–185 These variants lead to a buildup of acetaldehyde, a toxic alcohol metabolite that causes facial flushing, nausea, and tachycardia when alcohol is consumed.184,185 Although this response may limit heavier drinking, people who carry these variants are at increased risk for esophageal cancer even if they drink lightly.186 In addition to those of East Asian descent, people of other races and ethnicities can carry similar variants.187
    • Possible alcohol-cancer associations: While not conclusive, accumulating evidence suggests that alcohol consumption may be associated with increased risks of melanoma and prostate and pancreatic cancers. 181,188,189

    Chronic pain

    About 20% of adults in the U.S. have chronic pain, defined as pain most days in the past six months.190 Seeking relief, patients with chronic pain often self-medicate with alcohol.191

    • Alcohol and pain—a complex relationship: Significant pain relief is generally associated with reaching a blood alcohol concentration of approximately 0.08 percent, an intake equivalent to binge drinking (see drinking level terms, above).192 At the same time, heavy drinking can also cause or exacerbate painful conditions such as injuries, neuropathies, and pancreatitis, and if combined with opioid painkillers, can potentiate respiratory depression and overdose.193 (See Core article on medication interactions.) As with opioids, alcohol withdrawal produces hyperalgesia, or increased pain sensitivity, along with negative emotional states (also known as hyperkatifeia [hyper-kuh-TEE-fee-uh]) that further heighten both the hyperalgesia and the motivation to drink for physical and emotional pain relief.194,195 Heavy drinking to relieve pain can thus drive the development of AUD, and conversely, AUD-related changes in pain processing in the brain may drive the development of chronic pain conditions. 194,196
    • Helping patients who self-medicate with alcohol for pain: Advice from a healthcare professional to quit or cut back on drinking is likely to be more effective when both the drinking goals and the pain are addressed.191 In addition to managing pain through strategies such as physical therapy and exercise,192 patients may also benefit from pain-focused behavioral healthcare treatments, which include cognitive behavioral, mindfulness, and acceptance-based approaches.193 For patients in recovery from AUD, effective pain reduction during and after treatment may lower the risk of a return to heavy drinking.193

    See the Resources, below, for guidelines to help clinicians manage pain in patients with or in recovery from substance use disorders.

    Perioperative risk

    Heavy alcohol use and AUD are associated with increased surgical complications, whether from complications of alcohol withdrawal, abnormalities in hemostasis, wound healing, cardiopulmonary function, or interactions with medications.197–199 Chronic alcohol use may increase the dose requirements for general anesthetic agents.200 Small trials have shown reduced surgical complications from intensive programs that help patients reduce heavy alcohol use 1-3 months prior to surgery.201

    In closing, given that alcohol contributes to over 200 diseases and conditions, it is important to be aware that developing or worsening medical conditions in many patients may reflect an unrecognized alcohol problem. The health risks associated with alcohol reinforce the need for regular alcohol screening for all patients. When warranted, as part of a brief intervention, you can raise your patients’ awareness about their specific alcohol-related health consequences, which may help motivate them to cut back or quit as needed. (See Core article on brief intervention.)

    Resources

    Further Reading in the NIAAA Journal, Alcohol Research Current Reviews

    Cancer Care

    Chronic Pain Care

    Emergency Care

    Liver Care

    Prenatal Care and Fetal Alcohol Spectrum Disorders

    More resources for a variety of healthcare professionals can be found in the Additional Links for Patient Care.

    References

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    3. Alcohol [Internet]. World Health Organization. 2018 [cited 2022 Apr 13]. Available from: https://www.who.int/news-room/fact-sheets/detail/alcohol
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    7. Cao Y, Willett WC, Rimm EB, Stampfer MJ, Giovannucci EL. Light to moderate intake of alcohol, drinking patterns, and risk of cancer: results from two prospective US cohort studies. BMJ. 2015 Aug 18;351:h4238. PMCID: PMC4540790
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    Contributors

    Contributors to this article for the NIAAA Core Resource on Alcohol include the writer for the full article, the content contributors to subsections, reviewers, and editorial staff. These contributors included both experts external to NIAAA as well as NIAAA staff.

    External Writer

    Douglas Berger MD, MLitt
    Staff Physician, VA Puget Sound,
    Associate Professor of Medicine,
    University of Washington, Seattle, WA

    External Content Contributor

    Michael E. Charness, MD
    Chief of Staff, VA Boston Healthcare System;
    Professor of Neurology, Faculty Associate
    Dean, Harvard Medical School, Boston, MA

    NIAAA Content Contributors

    Bill Dunty, PhD
    Program Director, Division of Metabolism and
    Health Effects and FASD Research Coordinator, NIAAA

    Zhigang (Peter) Gao, MD
    Program Director, Division of
    Metabolism and Health Effects, NIAAA

    M. Katherine Jung, PhD
    Director, Division of Metabolism
    and Health Effects, NIAAA

    Lorenzo Leggio, MD, PhD
    NIDA/NIAAA Senior Clinical Investigator and Section Chief;
    NIDA Branch Chief;
    NIDA Deputy Scientific Director;
    Senior Medical Advisor to the NIAAA Director

    Svetlana Radaeva, PhD
    Deputy Director, Division of Metabolism and
    Health Effects, NIAAA

    Aaron White, PhD
    Senior Scientific Advisor to
    the NIAAA Director, NIAAA

    External Reviewers

    Majid Afshar, MD, MSCR
    Assistant Professor of Division of Allergy,
    Pulmonary and Critical Care Medicine,
    University of Wisconsin, Madison, WI

    Douglas Berger MD, MLitt
    Staff Physician, VA Puget Sound,
    Associate Professor of Medicine,
    University of Washington, Seattle, WA

    R. Colin Carter, MD, MMSc
    Associate Professor of Pediatrics in
    Emergency Medicine and Nutrition, Columbia
    University Vagelos College of Physicians and
    Surgeons, New York-Presbyterian Morgan
    Stanley Children’s Hospital, New York, NY

    Michael E. Charness, MD
    Chief of Staff, VA Boston Healthcare System;
    Professor of Neurology, Faculty Associate
    Dean, Harvard Medical School, Boston, MA

    Kenneth Lyons Jones, MD
    Distinguished Professor, Department of
    Pediatrics, University of California San Diego,
    La Jolla, CA

    Lewei (Allison) Lin MD, MS
    Assistant Professor, Department of
    Psychiatry, University of Michigan,
    Ann Arbor, MI

    Jessica L. Mellinger, MD MSc
    Assistant Professor, Gastroenterology,
    Internal Medicine, Transplant Hepatology,
    Michigan Medicine, Ann Arbor, MI

    Vijay H. Shah, MD
    Carol M. Gatton Chairman of Medicine,
    Mayo Clinic, Rochester, MI

    NIAAA Reviewers

    George F. Koob, PhD
    Director, NIAAA

    Patricia Powell, PhD
    Deputy Director, NIAAA

    Nancy Diazgranados, MD, MS, DFAPA
    Deputy Clinical Director, NIAAA

    Bill Dunty, PhD
    Program Director, Division of Metabolism and
    Health Effects and FASD Research Coordinator, NIAAA

    Mark Egli, PhD
    Deputy Director, Division of
    Neuroscience and Behavior, NIAAA

    Zhigang (Peter) Gao, MD
    Program Director, Division of
    Metabolism and Health Effects, NIAAA

    M. Katherine Jung, PhD
    Director, Division of Metabolism
    and Health Effects, NIAAA

    Lorenzo Leggio, MD, PhD
    NIDA/NIAAA Senior Clinical Investigator and Section Chief;
    NIDA Branch Chief;
    NIDA Deputy Scientific Director;
    Senior Medical Advisor to the NIAAA Director

    András Orosz, PhD
    Program Director, Division of Metabolism and Health Effects, NIAAA

    Aaron White, PhD
    Senior Scientific Advisor to
    the NIAAA Director, NIAAA

    Editorial Team

    NIAAA

    Raye Z. Litten, PhD
    Editor and Content Advisor for the Core Resource on Alcohol,
    Director, Division of Treatment and Recovery, NIAAA

    Laura E. Kwako, PhD
    Editor and Content Advisor for the Core Resource on Alcohol,
    Health Scientist Administrator,
    Division of Treatment and Recovery, NIAAA

    Maureen B. Gardner
    Project Manager, Co-Lead Technical Editor, and
    Writer for the Core Resource on Alcohol,
    Division of Treatment and Recovery, NIAAA

    Contractor Support

    Elyssa Warner, PhD
    Co-Lead Technical Editor,
    Ripple Effect

    Daria Turner, MPH
    Reference and Resource Analyst,
    Ripple Effect

    Kevin Callahan, PhD
    Technical Writer/Editor,
    Ripple Effect

    To learn more about CME/CE credit offered as well as disclosures, visit our CME/CE General Information page. You may also click here to learn more about contributors.

    Complete CME/CE Post-Test
    Last Revised

    niaaa.nih.gov

    An official website of the National Institutes of Health and the National Institute on Alcohol Abuse and Alcoholism

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