The Inflammatory Response to Alcohol Consumption and Its Role in the Pathology of Alcohol Hangover

Abstract

<jats:p>An increasing number of studies are focusing on the inflammatory response to alcohol as a potentially important determinant of hangover severity. In this article, data from two studies were re-evaluated to investigate the relationship between hangover severity and relevant biomarkers of alcohol metabolism, oxidative stress and the inflammatory response to alcohol. Hangover severity was significantly and positively correlated with blood concentrations of biomarkers of the inflammatory response to alcohol, in particular, Interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α) and C-reactive protein (CRP). At 4 h after alcohol consumption, blood ethanol concentration (but not acetaldehyde) was significantly and positively associated with elevated levels of IL-6, suggesting a direct inflammatory effect of ethanol. In addition, biomarkers of oxidative stress, i.e., malondialdehyde and 8-isoprostrane, were significantly correlated with hangover severity, suggesting that oxidative stress also contributes to the inflammatory response. The timing of the assessments suggests initial slow elimination of ethanol in the first hours after alcohol consumption. As a consequence, more ethanol is present in the second half of the night and the next morning, which will elicit more oxidative stress and a more profound inflammatory response. Together, these processes result in more severe hangovers.</jats:p>

Immune-Mediated Mechanisms in Cofactor-Dependent Food Allergy and Anaphylaxis: Effect of Cofactors in Basophils and Mast Cells

“…Ado, adenosine; green arrows, increase; red arrows, decrease. *Evidence based on references ( 23 , 26 , 28 , 29 , 38 , 39 , 41 , 50 , 57 – 59 , 66 , 67 ).…”

“…Alcohol has also been shown to increase histamine levels by inhibiting diamino oxidase (DAO), an enzyme that catabolizes histamine ( 65 ). It has also been described that alcohol induces pro-inflammatory mediator (such IL-6, IL-10, and IFN- γ ) release and eicosanoid metabolite production, such as PGE 2 ( 66 ). Similar to the hypothesis in FDEIA, food-dependent alcohol-induced anaphylaxis (FDAIA) patients could have a deficient production of PGE 2 .…”

Immune Responses after Heavy Alcohol Consumption: Cytokine Concentrations in Hangover-Sensitive and Hangover-Resistant Drinkers

“…Despite these functional consequences, the pathology of the alcohol hangover has received relatively little research attention. The immune system has been proposed to play a role in the pathology of the alcohol hangover [ 9 , 10 ]. It is hypothesized that cytokines are released as a response to alcohol intake and subsequently interact with the central nervous system (CNS), contributing to the various next-day symptoms collectively called the hangover state.…”

The Relationship between Pain Sensitivity, Pain Catastrophizing and Hangover Severity

“…The alcohol hangover has been defined as the combination of negative mental and physical symptoms which can be experienced after a single episode of alcohol consumption, starting when blood alcohol concentration (BAC) approaches zero [ 1 , 2 ]. Although alcohol hangover is the most frequently experienced negative consequence of alcohol consumption [ 3 ], scientific knowledge on the pathology of the alcohol hangover is limited [ 4 , 5 ].…”