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The Healthcare Professional's

Core Resource on Alcohol

Knowledge. Impacts. Strategies.

Medical Complications: Common Alcohol-Related Concerns

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    Step 2 - Complete the Brief Continuing Education Post-Test

    Takeaways

    • Alcohol is a leading cause of morbidity and mortality, with harms related to both acute and chronic effects of alcohol contributing to about 4.3 million emergency department visits and more than 178,000 deaths in the U.S. each year.
    • There are health risks even at low levels of alcohol consumption, including certain cancers and cardiovascular risks, regardless of the 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 per 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 challenges in managing other health conditions including hypertension, atrial fibrillation, diabetes, and recurrent lung infections.
    • Your patients may be unaware that their alcohol use may be contributing to their current medical problems and putting them at risk for future health issues. During brief interventions, you can help patients to see that they can improve their health and reduce risks by cutting back or quitting drinking.

    Alcohol’s harmful effects on multiple organs and body systems contribute to more than 200 health conditions,1,2 and alcohol-related mortality is on the rise.3,4 An estimated 178,000 people in the U.S. die from alcohol-related causes each year,4 making alcohol consumption one of the leading causes of preventable death.5 Approximately two thirds of alcohol-related deaths result from diseases and organ damage related to chronic heavy alcohol consumption while the remainder result from acute injuries sustained while intoxicated.4

    The health risks of alcohol tend to be dose-dependent, and the likelihood of certain harms begin at relatively low amounts.6,7 For example, even drinking within the current U.S. Dietary Guidelines (see drinking level terms below) can increase the risks of hypertension,8–12 arrythmias,13–16 and female breast cancer. 17–22 Overall, studies on alcohol and health underscore the message of "the less, the better" when it comes to alcohol consumption.16

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

    Acute harm and medical emergencies

    Emergency departments in the U.S. manage about 4.3 million alcohol-related visits on average each year.23 Acute alcohol-related medical emergencies and deaths can be the consequence of a single binge-drinking episode or long-term heavy drinking. Even low levels of alcohol use have been associated with increased risk of cardiovascular events (see “Cardiovascular system,” below).9,13,24

    Among the risks:

    • A single binge-drinking episode significantly increases the likelihood of motor vehicle crashes,25 atrial fibrillation,26 drownings,27 hypothermia,28,29 trauma in general,30–32 higher risk sexual behaviors and infections,33–37 falls, burns, and suicides,38,39 and overdoses from alcohol on its own or by potentiating overdose risk from other sedating drugs (see Core article on medication interactions).38,39
    • 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 problems40 including liver disease, pancreatitis, GI bleeding, and many other conditions listed below. Alcohol withdrawal accounts for approximately 260,000 emergency department visits41 and 850 deaths42 in the U.S. each year. For details about alcohol withdrawal, see the Core article on AUD.

    Note that screening and brief interventions for heavy alcohol use conducted in emergency departments show promise for reducing alcohol consumption after discharge.40 (See Core articles on screening and brief intervention.)

    Cancer

    Alcohol and its metabolite acetaldehyde are carcinogens linked with an increased risk for numerous cancers in humans. 43–46 Alcohol is the fourth largest modifiable risk factor for cancer in men and third largest for women, accounting for an estimated 5.4% of new cancer cases and 4.1% of cancer deaths in the U.S., according to a 2024 analysis.47 Yet, fewer than half of Americans recognize that alcohol is a risk factor for cancer. 48–50

    • 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.18,43,51 The harm appears to be independent of type of alcohol (beer, wine, liquor).44,45
      • Breast cancer: Even 1 drink per day is associated with a 5-15% increase in breast cancer risk compared to women who do not drink at all.17–22 Each year, more than 44,000 female breast cancer cases in the U.S., or about 16% of U.S. cases, are attributable to alcohol.47
      • Esophageal and head and neck cancers: People who drink heavily have five times the risk of developing esophageal and head and neck cancers compared to people who drink only occasionally or not at all.18 Some research indicates that even low-level alcohol consumption is associated with mouth and throat cancer.18,52
      • 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).53–56 These variants lead to a buildup of acetaldehyde, a toxic alcohol metabolite that causes facial flushing, nausea, and tachycardia when alcohol is consumed.55,56 Although this response may limit heavier drinking, people who carry these variants are still at increased risk for esophageal cancer even if they drink lightly.57 Although some people who carry the variant take antihistamines to lessen flush reaction symptoms while they continue to drink, this practice does not mitigate the increased cancer risk.55 In addition to those of East Asian descent, people of other races and ethnicities can carry similar variants.58
    • 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. 18,59,60

    Medical complications by individual body systems

    The following sections describe potential alcohol-related medical complications organized by specific body systems.

    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. Of note, a new diagnostic category called “MetALD” includes patients with a combination of ALD and metabolic syndrome, Type 2 diabetes, or other metabolic risk factors.61,62
      • 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 63
        • Steatosis, or fatty liver, is the earliest sign of liver injury and is present in about 95-100% of people who drink heavily.64 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.64
        • 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).65,66
        • 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, patients with alcohol-associated cirrhosis have an estimated annual incidence of developing primary hepatocellular carcinoma that ranges from 0.9% to 5.6%67 (see next bullet). Compared to men, women who drink alcohol have a greater risk for cirrhosis and their risk may increase even with low levels of consumption.68
        • Hepatocellular carcinoma (HCC) is the most common form of liver cancer, accounting for about 90% of cases.69 The majority of cases occur in people with chronic liver disease, with 15-30% of cases associated with alcohol-related cirrhosis.69 Research suggests that chronic alcohol use of greater than 80 g/day for more than 10 years increases the risk of HCC roughly 5-fold.70
        • Alcohol-associated hepatitis (AH) is a clinical syndrome that can develop suddenly in patients with longstanding heavy alcohol use and has been found in approximately 20% of people with alcohol use disorder (AUD).71–73 Rates of AH are rising rapidly, especially among women and those of lower socioeconomic status.73,74 AH is characterized by a rapid onset of jaundice, liver synthetic dysfunction, and hepatic decompensation.73 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.75 AH can occur in any stage of liver disease, and up to 80% of patients with severe AH may have underlying cirrhosis.76
      • 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 liver disorder requiring hospitalizations and transplants has increased markedly in the U.S. since the early 2000s, including among young adults.73,77–80 For example, the number of ALD patients listed for liver transplant increased by 63% from 2007 to 2017,77 and ALD is now the leading reason for liver transplantation in the country.73,81,82 Liver cirrhosis caused about 48,000 deaths nationwide in 2019, half of which were alcohol-related.83 The death rate for alcohol-related cirrhosis increased by 47% between 2000 and 2019, with greater increases for women (83.5%) than for men (33%).83
      • Abstinence is needed to improve the prognosis for ALD.66,84 Patients at any stage of ALD who have AUD should receive AUD treatment and be urged to maintain abstinence.85,86 (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.87,88
      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.89 Acute pancreatitis is a top reason for GI-related hospitalization in the U.S., with about 291,000 admissions annually.90 Up to 20% of these cases have serious complications that carry a mortality rate of 20-30%.91,92 Alcohol is the most common cause of hospital readmission after an episode of acute pancreatitis, potentially contributing to the progression to chronic disease.93 Smoking independently raises the risk for both types of pancreatitis and could synergize the effects of alcohol.94 Chronic pancreatitis can lead to pain, malabsorption, diabetes, pseudocysts, and pancreatic cancer.95 After an episode of alcohol-related pancreatitis, patients who reduce or abstain from alcohol markedly lower both the risk of recurrence and the risk of developing chronic pancreatitis.94 Therefore, identifying alcohol as the cause of pancreatitis is crucial for initiating alcohol counseling in at-risk patients.
    • 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.96–98 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.99,100 Over time, the inflammatory response triggered by these compounds contributes to damage to the liver, brain, and potentially other organs.100,101
      • 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.102 Alcohol also enhanced the risk of GI bleeds associated with aspirin or other NSAIDs. 102 Another study found that 1 in 5 patients hospitalized for GI bleeds drank heavily.103 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.103
    • 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.104 Drinking about one serving of alcohol per day is associated with a 16% increase in the risk of developing GERD.104

    Cardiovascular system

    • Blood pressure: Heavy alcohol consumption is linked with elevated systolic and diastolic blood pressure,107 and among people who drink heavily, reducing alcohol intake lowers blood pressure in a dose-dependent manner.108 Even low level alcohol consumption (1 to 2 drinks per day) is associated with increased blood pressure,9,11 seemingly independent of other common lifestyle factors such as diet, exercise, and medication adherence,12 although there may be some difference by sex.9,9,11
    • 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.26 Even less than one drink per day is associated with an increased risk of developing AF.13 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.”26 Moreover, chronic heavy alcohol consumption is associated with an increased likelihood of developing AF over time.109 In patients with a history of AF, reducing alcohol consumption to near-abstinence levels may lower the risk of recurrence of AF,26 although some research indicates that any alcohol use raises the risk for an AF episode in the hours that follow consumption.15
    • Cardiomyopathy: Chronic heavy alcohol consumption can cause cardiomyopathy leading to progressive reduction in heart muscle contractility and heart chamber dilation.110–113 Abstinence or reductions in consumption are associated with improvements in heart health in patients with cardiomyopathy.114
    • Myocardial infarction and stroke: Heavy, long-term alcohol use increases the risk of heart attack and stroke.6,115 A mounting body of evidence indicates that even low-level drinking offers no cardiovascular protection and may increase the risk of stroke.8,10,106,116

    Neurological system

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

    Neurological 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.117 Heavy drinking can alter the trajectory of adolescent brain development118–120 and contributes to dementia in older drinkers.117,121–125 Heavy alcohol use over time damages the brain through a combination of direct neurotoxic effects, nutritional deficiencies, neuroinflammation, liver disease, and metabolic abnormalities,122,126 all exacerbated by aging.127 Alcohol neurotoxicity reduces synaptic complexity, 123,124 alters communication between nerve cells, 123,124 and decreases brain volume,125 particularly in frontal regions.117,122 Brain damage due to alcohol can manifest in problems with attention, memory, and reasoning.117 Abstinence may partially reverse these changes.128 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.129–131 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.132,133 Abstinence may lead to improvement of symptoms.134
    • Wernicke’s encephalopathy: Severe AUD can result in reduced food intake and malabsorption of thiamine, which leads to thiamine deficiency.135 In turn, thiamine deficiency can cause Wernicke’s encephalopathy (WE).136,137 Often underdiagnosed, WE is a treatable neurologic emergency affecting both the central and peripheral nervous systems.138 Any symptoms of WE in patients with AUD—such as mental confusion, vision problems, gait coordination problems, hypothermia, low blood pressure, lethargy, or coma139—should prompt immediate parenteral thiamine treatment.140,141 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,142–144 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.141,145,146 A majority of patients with KS require prolonged institutional care.147 Some degree of recovery may occur over many months and is dependent on treatment of nutritional deficiencies and abstinence from alcohol.128,148,149 Studies have not demonstrated a beneficial effect from pharmacological therapy, but memory rehabilitation programs have shown promising results.150,151

    Endocrine system

    Heavy alcohol use has the potential to disrupt the endocrine system’s many chemical pathways that normally help maintain homeostasis and health.152

    • 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.152 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.152 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 adequately153–155 and thus contributes to the progression of diabetes-associated cardiovascular and neurologic complications.154,156,157 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 sensitivity2 —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.158 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.159

    • 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.160 When hospitalized with pneumonia, patients with alcohol-related problems, particularly those in withdrawal, are at increased risk of poor outcomes.161,162
    • Acute Respiratory Distress Syndrome(ARDS): Long-term heavy drinking raises the risk for respiratory infections and for ARDS,163 with increased need for mechanical ventilation, prolonged stays in the intensive care unit, and greater mortality.164–166 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.163,167
    • 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,168 and in these cases, the effects of heavy drinking on the immune system may exacerbate the ARDS and worsen the prognosis. 

    Immune system

    Both acute and chronic heavy use of alcohol can interfere with multiple aspects of the immune response,158,169,170 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.159

    • 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,171–174 and thus may reduce the ability of the innate immune system to fight infections.99 Chronic alcohol exposure can impair wound healing and increase the incidence of wound infection.175
    • 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.96,176 Chronic alcohol consumption increases levels of circulating pro-inflammatory cytokines, potentially adding to inflammation caused by disease or natural aging.177,178 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 ARDS (see Pulmonary System section above).179,180

    For more on this topic, see articles from the NIAAA journal issue on Alcohol and the Immune System.181

    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.182

    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. 183,184 These chronic alcohol-related myopathies affect approximately 50% of patients with AUD,185 and occur far more frequently than inherited myopathies. In contrast, acute alcohol-related myopathies affect approximately 1-2% of patients with AUD 185,186 and can occur following a single severe binge drinking episode. 185,186
    • 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.187,188 Alcohol can disrupt the balance between the erosion and remodeling of bone tissue, contributing to decreased bone density and increased risk of fracture.189 Among those who drink heavily, it is likely that falls contribute to the increased fracture risk.188 Even people who drink less than heavily are significantly more likely to be injured in falls than people who do not drink.190
    • 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.191 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.192 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.192

    Hematological system

    Heavy alcohol use can cause anemia, leukopenia, and thrombocytopenia as well as macrocytosis. 193,194 It is unclear to what extent these abnormalities are caused directly by marrow toxicity or indirectly by liver disease, hypersplenism, and nutritional deficiencies.193,194

    Prenatal alcohol exposure

    Prenatal alcohol exposure can cause lifelong physical, behavioral, and cognitive impairments collectively known as fetal alcohol spectrum disorders (FASD), a leading cause of intellectual disability and birth defects in the U.S. 195–197 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.195,198–201Even lower levels of alcohol exposure during pregnancy are associated with increased risks for miscarriage,202 and for adverse behavioral and psychological outcomes in children.203 And the risk for Sudden Infant Death Syndrome (SIDS) and late stillbirth is elevated with continued drinking beyond the first trimester, and increases further when combined with smoking.204,205
    • Advice to abstain during pregnancy: Obstetric and pediatric guidelines advise maternal abstinence from drinking alcohol throughout pregnancy.195,206,207 Moreover, the U.S. Surgeon General recommends that women who are considering becoming pregnant abstain from alcohol.208
    • Multiple disorders: FASD encompasses a range of possible disorders based on the type and degree of impairments.195,196,206 Included are the following disorders, each defined by specific features:
      • Fetal Alcohol Syndrome (FAS) is characterized by structural or functional central nervous system abnormalities, growth deficits, and facial anomalies, which may include narrow eye openings, a smooth area between the lip and the nose, and a thin upper lip.
      • Partial Fetal Alcohol Syndrome (pFAS) is characterized by some, but not all, of the features of FAS. For example, individuals with pFAS may not experience growth deficits.
      • Alcohol-Related Neurodevelopmental Disorder (ARND) is diagnosed in individuals who do not exhibit the full range of physical deficits that characterize FAS or pFAS, but who do have cognitive, behavioral, and central nervous system deficits.
      • Alcohol-Related Birth Defects (ARBD) is characterized by physical abnormalities, such as heart, kidney, and skeletal problems. ARBD is rarely seen alone but rather as a secondary disorder accompanying other forms of FASD.
      • Neurobehavioral Disorder Associated with Prenatal Alcohol Exposure (ND-PAE) is defined only by cognitive and behavioral features and is characterized specifically by impairments in neurocognition, self-regulation, and adaptive functioning.
    • Estimated prevalence of prenatal alcohol exposure and FASD: About 1 in 12 pregnant women in the U.S. report drinking, and among them, almost half report binge drinking.211 There has been a slightly increasing trend from 2011 to 2020 in current and binge drinking during pregnancy.212 An estimated 1-5% of first-grade children in the U.S. have FASD, which is comparable to or even more common than the prevalence of autism spectrum disorder.196,213
    • 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.214 Milder forms of FASD may cause subtle neurodevelopmental effects that do not prompt clinical attention.196 Note that central nervous system deficits may be attributed to other conditions, and FASD remains under-diagnosed, in part, because only a minority of individuals with FASD have facial dysmorphology.196
    • 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 more challenging.215 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.216

    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.

    Chronic pain

    About 20% of adults in the U.S. have chronic pain, defined as pain most days in the past six months.217 Seeking relief, patients with chronic pain often self-medicate with alcohol.218 However, prolonged alcohol use can exacerbate pain sensitivity and interfere with pain management, creating a vicious cycle that is challenging to break.219

    • Alcohol and pain—a complex, bidirectional relationship: Significant acute pain relief is generally associated with reaching a blood alcohol concentration of approximately 0.08%, an intake equivalent to binge drinking (see drinking level terms, above).220 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.221 (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.222,223 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. 222,224
    • 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.218 In addition to managing pain through strategies such as physical therapy and exercise,220 patients may also benefit from pain-focused behavioral healthcare treatments, which include cognitive behavioral, mindfulness, and acceptance-based approaches.221 For patients in recovery from AUD, effective pain reduction during and after treatment may lower the risk of a return to heavy drinking.221
    • Integrated treatment approaches. Simultaneously addressing AUD and chronic pain can enhance treatment outcomes for patients grappling with both conditions. Coordinated care between pain management and addiction specialists can provide comprehensive support. Further, some pharmacotherapies for AUD have analgesic potential. The medications gabapentin and topiramate, for example, are commonly used for neuropathic pain and are recommended by the American Psychiatric Association as second-line, off-label options to treat AUD in patients who have not responded to the FDA-approved AUD medications naltrexone and acamprosate. 219,225 (See Core article on treatment.) Although further research is needed, potentially dual-action drugs may offer a streamlined approach to managing both chronic pain and AUD while improving treatment adherence and outcomes.219

    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.226–228 Chronic alcohol use may increase the dose requirements for general anesthetic agents.229 Small trials have shown reduced surgical complications from intensive programs that help patients reduce heavy alcohol use 1-3 months prior to surgery.230

    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, and that an alcohol problem may be a window on the etiology or exacerbation of a medical condition. 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

    Gastroenterology and Hepatology

    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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    *Lorenzo Leggio, MD, PhD
    Clinical Director and Deputy Scientific Director, NIDA;
    Branch Chief and Senior Investigator, NIDA/NIAAA,
    NIH Intramural Research Program, Baltimore, MD

    *Svetlana Radaeva, PhD
    Former 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 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 Nutrition and
    Emergency Medicine, Department of Pediatrics
    and Emergency Medicine, Institute of Human Nutrition,
    Columbia University Irving Medical Center;
    Attending Physician, NewYork-Presbyterian
    Morgan Stanley Children's Hospital,
    Columbia University College of
    Physicians and Surgeons, New York, NY

    Michael E. Charness, MD
    Chief of Staff, VA Boston Healthcare System;
    Professor of Neurology and 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
    Associate Professor, Department of Psychiatry,
    University of Michigan Medical School, Ann Arbor, MI

    *Jessica L. Mellinger, MD MSc
    Assistant Professor, Henry Ford Health,
    Michigan State University, Detroit, MI

    *Vijay H. Shah, MD
    Ronald F. Kinney Executive Dean of Research;
    Carol M. Gatton Professor of Medicine, Physiology, and
    Cancer Cell Biology,
    Mayo Clinic, Rochester, MN

    NIAAA Reviewers

    *George F. Koob, PhD
    Director, NIAAA

    *Patricia Powell, PhD
    Deputy Director, NIAAA

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

    *William C. Dunty, Jr., PhD
    Program Director and FASD Research Coordinator,
    Division of Metabolism and Health Effects, 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
    Clinical Director and Deputy Scientific Director, NIDA;
    Branch Chief and Senior Investigator, NIDA/NIAAA,
    NIH Intramural Research Program, Baltimore, MD

    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;
    Former Director,
    Division of Treatment and Recovery, NIAAA

    *Laura E. Kwako, PhD
    Editor and Content Advisor for
    The Core Resource on Alcohol;
    Chief, Treatment, Health Services, and Recovery Branch;
    Credentialed Clinician (Psychologist),
    Division of Treatment and Recovery, NIAAA

    *Maureen B. Gardner
    Project Manager and Technical Writer/Editor for
    The Core Resource on Alcohol,
    Division of Treatment and Recovery, NIAAA

    *Erin H. Bryant
    Project Manager and Technical Writer/Editor 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

    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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