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Alcohol: Reducing the Risks

How Alcohol Causes Hangover Symptoms

The specific mechanisms that cause hangover symptoms to manifest are not completely understood, although an important clue is that the symptoms remain after the alcohol itself is no longer in circulation. Thus, residual effects such as inflammation, altered immune function, and oxidative damage appear likely to be key contributors to hangover as well as other systemic impacts of alcohol overconsumption (Penning 2010; McCarty 2013; Verster 2008; Gonzalez-Reimers 2014).


In addition to exerting direct toxicity on gastrointestinal cells, alcohol causes an increase in permeability of the intestinal lining, which allows toxins present in the intestine (endotoxin) to pass into the bloodstream. This gives rise to an inflammatory immune response with effects throughout the body (Gonzalez-Reimers 2014; Kawaratani 2013). Evidence from animal research suggests the combination of alcohol and endotoxin can quickly raise levels of inflammatory cytokines in the blood, liver, and brain (Gonzalez-Reimers 2014). The action of these cytokines in the central nervous system has been linked to hangover-like symptoms in animal models (Dantzer 2007).

Alcohol may further contribute to inflammation by stimulating the activity of enzymes that accelerate production of inflammatory prostaglandins. In addition, oxidizing enzymes induced by alcohol generate increased levels of free radicals (Gonzalez-Reimers 2014). Combined with the free radicals produced during alcohol metabolism, this high oxidative load contributes to the vicious cycle of cellular injury and inflammatory signaling (Kawaratani 2013; McCarty 2013; Biswas 2016), which may contribute to both the acute and chronic consequences of excessive alcohol consumption (McCarty 2013).

Other Theories

Although popular wisdom holds that dehydration is a major contributor to hangover, research has failed to find an association between markers of dehydration and hangover severity (Penning 2010). Similarly, while many people suspect that alcohol-induced hypoglycemia leads to hangover, changes in blood glucose levels during alcohol ingestion are affected by many factors and circumstances, and a relationship between hypoglycemia and hangover has not been clinically verified (Prat 2009). Another hypothesis that awaits exploration suggests that the cognitive and psycho-emotional symptoms of hangover are related to a disturbance in neurotransmitter systems caused by an acute form of alcohol withdrawal (Prat 2009; Piasecki 2010; Costardi 2015).

A group of compounds found in alcoholic beverages, called congeners, have been proposed to contribute to hangover symptoms. Congeners are molecules produced during fermentation and distillation, or added to alcohol to enhance flavor, aroma, and color. They are widely present in alcoholic beverages in very small amounts, with darker spirits and red wine generally containing more congeners than lighter spirits, white wine, and beer (Verster 2008; Prat 2009). Certain congeners and their metabolites appear to act as toxins (Prat 2009; Rohsenow, Howland 2010; Verster 2008). Although the possible relationship between congeners and hangover is not yet fully understood, drinking high-congener alcohol, compared with low-congener alcohol, has been correlated with increased severity of hangover in several preliminary studies. Nevertheless, hangovers can result from excessive intake of any alcohol, regardless of its congener content (Verster 2008; Prat 2009).

Several individual factors can influence hangover severity, including:

  • Age. Adolescents and young adults experience more frequent and severe hangovers (Tolstrup 2014; Huntley 2015).
  • Genetics. Genetic variability and other individual differences affect how alcohol is metabolized (Slutske 2014).
  • Smoking. Smoking is associated with increased hangover likelihood and severity (Jackson 2013).
  • Medications. Many medications can impact the risk of intoxication and hangover by influencing alcohol metabolism (Cederbaum 2012).

It is also interesting to note that patients who have had gastric bypass surgery (usually a treatment for obesity) may have altered alcohol metabolism, with faster absorption and slower metabolism. These patients are thought to be at higher risk of developing alcohol use disorder (Wee 2014), and could potentially have a greater chance of experiencing hangover.

Alcohol and Diabetes

Low levels of alcohol consumption appear to protect against diabetes, but consuming high levels increases risk for diabetes and its complications (Steiner 2015; Zhou 2016; Munukutla 2016). The type of alcohol consumed may also be important, as beer and wine have been found to be associated with reduced diabetes risk. Specific phytochemicals in beer and wine, including polyphenols, may explain some of this risk reduction. The apparent positive effects of low and moderate alcohol intake on diabetes risk and complications may be due to improvement in insulin sensitivity and increased anti-inflammatory activity (Zhou 2016).

Heavy alcohol intake, conversely, has been shown to increase levels of inflammatory markers and cause a deterioration of insulin sensitivity. It may also cause insulin secretion to diminish due to pancreatic damage (Zhou 2016). A regular habit of drinking approximately four alcoholic drinks (50–60 grams of alcohol) per day has been linked to increased diabetes risk (Steiner 2015), and can raise the likelihood of complications in diabetics. Diabetics who drink excessively increase their risk of heart disease and heart attack, kidney disease and kidney failure, and cirrhosis (Munukutla 2016).  

The Dangers of Combining Alcohol with NSAIDs or Acetaminophen

Some over-the-counter remedies often used to ease some hangover symptoms, such as acetaminophen (Tylenol), ibuprofen, or aspirin, may increase the negative effects of alcohol. Alcohol and non-steroidal anti-inflammatory drugs (NSAIDs) like aspirin and ibuprofen irritate the gastric lining and can cause gastrointestinal bleeding, and the risk of bleeding is exacerbated when they are used together (Moore 2015).

In one study, the risk of gastrointestinal bleeding was 2.7-fold higher in people who took any dose of ibuprofen regularly and drank any amount of alcohol in the week prior to the bleeding episode. The combined effect of alcohol and aspirin was even more dramatic: In those who used aspirin at least every other day at doses of 325 mg per day or lower, the risk of gastrointestinal bleeding was 2.8 times higher if they drank any amount of alcohol, and in those who used more than 325 mg per day of aspirin, alcohol use increased their risk 7-fold (Kaufman 1999).  

Acetaminophen is an analgesic often preferred to NSAIDs because of its relative safety with regard to gastrointestinal bleeding (ACG 2016). Because of its high potential for liver toxicity, however, it is not safe when combined with alcohol (Mayo Clinic 2014; UMMC 2015; Suzuki 2009). Furthermore, acetaminophen has been shown to interfere with alcohol metabolism (Lee, Liao 2013) and may contribute to greater alcohol sensitivity.