Alcohol and Inflammation: What the Research Shows (2026)

Chronic inflammation is a driver of heart disease, type 2 diabetes, autoimmune disorders, and depression. Research over the past decade has painted a clear, nuanced picture: alcohol's effect on inflammation is real and measurable, and the outcome depends heavily on how much you drink and what you choose to drink.

Last updated: April 2026

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Table of Contents

• How Alcohol Triggers Inflammation
• Key Inflammatory Markers Affected by Alcohol
• Red Wine, Beer, and Spirits: Which Drink Causes the Most Inflammation?
• The Science Behind Alcohol and Gut Health
• Moderate Drinking: Where the Research Gets Complicated
• Alcohol, Sleep, and the Inflammation Connection
• Practical Guidelines for an Anti-Inflammatory Lifestyle
• Frequently Asked Questions
• Sources & Methodology

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How Alcohol Triggers Inflammation

Inflammation is your body's first-line immune response — a cascade of biological signals designed to protect you from infection and injury. When functioning properly, this acute inflammatory response is self-limiting and resolves once the threat has passed.

Alcohol, however, disrupts this carefully regulated system in multiple ways.

When you consume alcohol, it is absorbed primarily through the stomach and small intestine and travels to the liver, where it is metabolised by enzymes including alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH). This metabolic process generates acetaldehyde — a toxic intermediate compound that is significantly more reactive than alcohol itself. Acetaldehyde causes direct damage to proteins, DNA, and cellular membranes throughout the body.

The body's response to this damage is to activate its inflammatory immune machinery. White blood cells called macrophages and Kupffer cells (the liver's resident immune cells) recognize alcohol and its metabolites as foreign substances and release inflammatory signaling molecules called cytokines. These cytokines — including interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) — recruit additional immune cells to the site of perceived damage, triggering a cascade of inflammatory activity.

This process happens every time you drink, regardless of the amount. The critical differences lie in magnitude and duration. A single drink triggers a mild, short-lived inflammatory response in most people — analogous to the body's response to a minor injury. Multiple drinks or chronic drinking shifts the body into a state of systemic low-grade chronic inflammation, where inflammatory signals persist continuously, damaging tissues and organs over time.

The research supporting this mechanism is robust. A landmark study published in the Journal of Hepatology demonstrated that even moderate alcohol consumption elevates circulating inflammatory markers within hours of ingestion, with the effect size correlating directly with the amount consumed. The researchers concluded that there is no completely safe threshold for alcohol's inflammatory effects, though very light drinking produces effects so minimal they may not carry significant clinical consequences for most healthy individuals.

Chronic systemic inflammation driven by alcohol does not remain confined to one organ. Sustained elevations in inflammatory cytokines affect the brain, joints, cardiovascular system, gut, and liver — creating the physiological foundation for the diseases most strongly associated with alcohol-related mortality. For people managing tinnitus or sound sensitivity, this is particularly relevant: research has linked chronic inflammation in the auditory system to tinnitus development and persistence, a connection explored in detail in the guide to inflammation and tinnitus at our partner resource.

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Key Inflammatory Markers Affected by Alcohol

Researchers measure alcohol's inflammatory effects through specific biomarkers found in blood samples. Understanding these markers gives you a concrete sense of what drinking actually does inside your body.

C-Reactive Protein (CRP)

CRP is one of the most widely studied inflammatory markers in alcohol research. Produced by the liver in response to inflammatory cytokines, CRP rises rapidly during acute inflammation and serves as a general indicator of systemic inflammatory activity.

Multiple large-scale studies have documented a J-shaped relationship between alcohol consumption and CRP levels. Light to moderate drinkers tend to have slightly lower CRP levels than abstainers — an effect attributed to the anti-inflammatory compounds in certain alcoholic beverages, particularly red wine. However, as consumption increases, CRP levels rise sharply, with heavy drinkers showing significantly elevated CRP compared to both moderate drinkers and teetotallers.

A 2023 meta-analysis in Alcoholism: Clinical and Experimental Research examining data from over 120,000 participants confirmed this pattern and noted that binge drinking episodes caused acute CRP spikes that took up to 24 hours to return to baseline.

Interleukin-6 (IL-6)

IL-6 is a pro-inflammatory cytokine that plays a central role in the immune system's inflammatory signaling network. It is produced by immune cells, endothelial cells lining blood vessels, and fat cells (adipocytes).

Research consistently shows that acute alcohol exposure increases IL-6 production. A controlled experimental study published in Alcohol had participants consume a standardised alcohol dose and found IL-6 levels rose by approximately 40% within 90 minutes, with levels remaining elevated for several hours. Chronic heavy drinking is associated with consistently elevated IL-6, which is particularly concerning because persistently high IL-6 is linked to insulin resistance, bone resorption, and cardiovascular disease risk.

Tumor Necrosis Factor-Alpha (TNF-α)

TNF-α is another key pro-inflammatory cytokine, primarily produced by macrophages. It plays a crucial role in the inflammatory response to infection and injury but becomes damaging when produced chronically.

Heavy alcohol consumption is strongly associated with elevated TNF-α levels. In the liver, increased TNF-α production by Kupffer cells is a primary driver of alcoholic liver disease — progressing from simple fatty liver (steatosis) through hepatitis to cirrhosis. A 2024 study in Hepatology documented that TNF-α levels in heavy drinkers correlated directly with the severity of liver inflammation and fibrosis.

Nuclear Factor Kappa B (NF-κB)

NF-κB is not a biomarker you will find on a standard blood test, but it is arguably the most important mechanism in alcohol-induced inflammation at the cellular level. NF-κB is a transcription factor — a protein that controls which genes are switched on in a cell. When activated by alcohol or inflammatory signals, NF-κB moves from the cell's cytoplasm into its nucleus and switches on genes responsible for producing inflammatory cytokines, including IL-6 and TNF-α.

In other words, NF-κB is the master switch that amplifies alcohol's inflammatory effects throughout the body. Research published in Cellular Immunology and other journals has shown that alcohol activates the NF-κB pathway in multiple cell types, including immune cells, liver cells, brain cells, and the epithelial cells lining the gut.

Comparison of Inflammatory Effects by Alcohol Type

The table below summarises how different alcoholic beverages affect key inflammatory biomarkers, based on the best available clinical evidence.

Beverage Type	CRP Effect	IL-6 Effect	TNF-α Effect	Gut Impact	Recommendation
Red Wine (moderate)	Mild increase or neutral; polyphenols may blunt rise	Mild, transient increase	Mild increase	Moderate disruption; polyphenols offer some gut protection	Best option if choosing to drink; limit to 1 glass/day max
White Wine	Moderate increase	Moderate increase	Moderate increase	Moderate disruption; minimal polyphenol protection	Limited anti-inflammatory benefit; consider alternatives
Beer (moderate)	Neutral in some studies; dose-dependent	Mild to moderate increase	Moderate increase	Moderate disruption; hops polyphenols offer marginal benefit	Neutral to mildly inflammatory; avoid binge drinking
Spirits (vodka, whiskey, gin, rum)	Significant acute increase	Large acute increase	Significant increase	Severe rapid disruption; high ABV damages gut barrier quickly	Most inflammatory; strongly discourage for inflammatory conditions
Abstinence / Near-Abstinence	Baseline	Baseline	Baseline	Intact gut barrier; healthy microbiome	Optimal for managing inflammatory conditions

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Red Wine, Beer, and Spirits: Which Drink Causes the Most Inflammation?

Not all alcoholic beverages affect inflammation equally. The type of drink matters significantly, and this is one of the most important nuances in the science.

Red Wine: The Most Studied Case

Red wine has received the most research attention of any alcoholic beverage regarding inflammation, largely because of the French Paradox — the observation in the 1990s that French populations consumed relatively high amounts of saturated fat yet had lower rates of heart disease than expected. Researchers hypothesised that red wine's polyphenols, particularly resveratrol, might confer cardiovascular protection through anti-inflammatory mechanisms.

Resveratrol is a natural compound produced by grape vines in response to stress, injury, or fungal infection. In laboratory studies, resveratrol has demonstrated:

• Inhibition of NF-κB activation
• Suppression of TNF-α and IL-6 production
• Activation of AMPK and sirtuin pathways associated with longevity
• Antioxidant effects that reduce oxidative stress

However, resveratrol research in humans tells a more complicated story. While red wine does contain resveratrol, the concentrations achieved in human blood after drinking are significantly lower than those used in laboratory cell and animal studies. Human trials of resveratrol supplementation have produced inconsistent results, with most showing minimal anti-inflammatory benefit at realistic dietary doses.

The current scientific consensus, as summarised in a 2024 review in Antioxidants & Redox Signaling, is that red wine's alcohol content likely cancels out or at least significantly diminishes any anti-inflammatory benefit from its polyphenols. At moderate consumption (1 glass per day for women, 2 for men), any positive or neutral effect is modest at best. At higher consumption levels, the inflammatory harms of alcohol clearly outweigh any polyphenol benefits.

White Wine

White wine contains far less resveratrol and other polyphenols than red wine because it is fermented without grape skins. What remains are the simpler phenolic compounds from the grape pulp and, in some styles, oak aging. The anti-inflammatory argument that applies (tentatively) to red wine does not apply meaningfully to white wine. From an anti-inflammatory perspective, white wine is best considered as a source of alcohol with no significant offsetting benefit.

Beer

Beer presents a more complex picture. Like wine, beer contains bioactive compounds from its raw ingredients — notably polyphenols from hops (including xanthohumol, which has demonstrated anti-inflammatory and anticancer properties in laboratory studies) and phenolic compounds from malted barley.

A 2022 study published in the European Journal of Clinical Nutrition compared the inflammatory profiles of moderate beer and wine drinkers over a 12-week period. The study found that moderate beer consumption did not significantly elevate CRP or IL-6 in healthy participants, though the researchers noted that the study was funded in part by a beer industry organisation and called for independent replication.

Other research tells a less favourable story. The alcohol content in beer, regardless of its polyphenol content, still activates NF-κB and triggers the gut-liver inflammatory cascade described earlier. Beer consumed in large quantities — as is culturally common with many pint-sessions — causes the same inflammatory damage as other forms of alcohol.

Spirits (Vodka, Whiskey, Gin, Rum)

Spirits are the most inflammatory category of alcoholic beverage in most studies. Because spirits contain a higher concentration of alcohol by volume (40% ABV or more compared to 12-14% for wine and 4-8% for beer), the dose of alcohol delivered per standard drink is higher. A standard 1.5 oz shot of spirits delivers the same pure alcohol as a 5 oz glass of wine or a 12 oz beer — but in a much smaller volume, which means it reaches the stomach and intestines more rapidly in a more concentrated form.

Rapid alcohol delivery to the small intestine appears to amplify the damage to the gut barrier. Several studies have directly compared the inflammatory effects of spirits versus wine or beer, consistently finding that spirits produce larger acute inflammatory responses, as measured by post-consumption cytokine levels.

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The Science Behind Alcohol and Gut Health

One of the most important — and least discussed — mechanisms of alcohol-induced inflammation involves the gut. This connection, sometimes called the gut-liver axis or gut-inflammatory axis, is a major pathway through which even moderate alcohol consumption affects whole-body inflammation.

The gastrointestinal tract is home to trillions of microorganisms collectively called the gut microbiome, which plays a crucial role in immune function, digestion, and the maintenance of the intestinal barrier. This barrier is a single layer of epithelial cells separated by tight junctions — protein complexes that seal the spaces between cells and prevent the contents of the gut (including bacteria, food particles, and digestive enzymes) from entering the bloodstream.

Alcohol disrupts this barrier in multiple ways:

Damage to intestinal epithelial cells. Alcohol and its metabolite acetaldehyde are directly toxic to the cells lining the intestine. Studies using human intestinal cell cultures have shown that alcohol exposure causes these cells to undergo programmed cell death (apoptosis), weakening the structural integrity of the gut lining.

Disruption of tight junction proteins. Alcohol reduces the expression and function of key tight junction proteins including zonula occludens-1 (ZO-1) and occludin. When these proteins are compromised, the tight junctions become "leaky" — allowing substances to pass through that would normally be blocked.

Alteration of the gut microbiome. Chronic alcohol consumption changes the composition of the gut microbiome, reducing the diversity of beneficial bacterial species and allowing overgrowth of potentially harmful bacteria. These changes further compromise gut barrier function and contribute to inflammation.

The consequences of this gut barrier dysfunction are significant. When the intestinal barrier becomes permeable, bacterial endotoxins — most notably lipopolysaccharide (LPS) — enter the bloodstream. LPS is a component of the outer membrane of Gram-negative bacteria. Once in the circulation, LPS is recognized by the immune system as a sign of infection, triggering a potent inflammatory response.

This phenomenon is sometimes called endotoxemia — the presence of endotoxins in the blood. Elevated blood endotoxin levels after alcohol consumption have been documented in multiple human studies. Once endotoxins reach the liver, they activate Kupffer cells (the liver's resident macrophages), which respond by releasing large amounts of IL-6 and TNF-α. This creates a self-perpetuating cycle of inflammation that extends from the gut to the liver and throughout the body.

The implications extend well beyond the digestive system. Research has linked alcohol-induced gut permeability to:

• Metabolic inflammation and insulin resistance
• Neuroinflammation contributing to anxiety, depression, and cognitive decline
• Systemic inflammation affecting joints, skin, and cardiovascular tissue
• Alcoholic liver disease progression

If you are managing an inflammatory condition — whether arthritis, autoimmune disease, psoriasis, or chronic gut issues — maintaining gut barrier integrity is essential. Alcohol actively works against this goal.

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Moderate Drinking: Where the Research Gets Complicated

Much public health messaging around moderate drinking and health has been called into question in recent years. A major 2023 study published in The Lancet challenged the longstanding claim that moderate alcohol consumption protects against cardiovascular disease, arguing that previous observational studies suffered from methodological flaws — most notably, comparing moderate drinkers to a heterogeneous group of "non-drinkers" that included many former drinkers who quit due to health problems, making moderate drinkers appear healthier by comparison.

When studies properly account for these biases, the cardioprotective effect of moderate drinking — if it exists at all — becomes much smaller and less certain. The inflammatory angle is similarly complicated.

What the Evidence Supports

The evidence that heavy drinking causes significant, measurable inflammation is strong and consistent. Studies of heavy drinkers (those consuming 4+ drinks per day consistently) show markedly elevated inflammatory markers across virtually all measured biomarkers.

The evidence that binge drinking (consuming 4+ drinks in a single session for women, 5+ for men) causes acute inflammation is also clear. Binge drinking episodes produce a demonstrable inflammatory response that peaks approximately 6-12 hours after consumption and can take up to 24 hours to fully resolve.

What Remains Uncertain

The evidence for light to moderate drinking (1-2 drinks per day) is genuinely uncertain. Some studies show slightly elevated inflammatory markers in this group compared to abstainers; others show no significant difference. A small number of studies — primarily of red wine — show modest anti-inflammatory effects.

The honest answer based on current evidence is that the inflammatory impact of light to moderate drinking varies between individuals and likely depends on:

• Genetic factors affecting alcohol metabolism (particularly ADH and ALDH enzyme variants)
• Baseline inflammatory status (a person with existing chronic inflammation may be more sensitive to alcohol's effects)
• Sex and hormonal factors (women generally experience more pronounced inflammatory effects from equivalent alcohol doses than men)
• Dietary context (drinking with food, particularly anti-inflammatory foods, may blunt some effects)
• Overall health status (individuals with liver disease, autoimmune conditions, or metabolic disorders are likely more sensitive to alcohol's inflammatory effects)

This uncertainty is not a green light for moderate drinking as a health strategy. It means that if you do drink, staying within the most conservative guidelines (no more than 1 drink per day for either sex, and ideally several alcohol-free days per week) is the most defensible approach from an inflammation perspective.

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Alcohol, Sleep, and the Inflammation Connection

Sleep and inflammation are deeply interconnected. Poor sleep increases inflammation; inflammation disrupts sleep. Alcohol affects both, creating a bidirectional negative cycle that compounds inflammatory damage.

While alcohol is often perceived as helping with sleep onset — it is a central nervous system depressant that can make you feel drowsy — it significantly disrupts sleep quality and architecture. The Sleep Foundation and multiple peer-reviewed studies document the following effects:

Reduced REM sleep. REM (Rapid Eye Movement) sleep is the stage of sleep most associated with memory consolidation, emotional processing, and brain detoxification. Alcohol reduces REM sleep duration, particularly in the second half of the night when the body is metabolising the alcohol and experiencing rebound effects.

Increased wakefulness. Alcohol fragments sleep, causing more frequent awakenings throughout the night. These micro-awakenings, often not consciously remembered, prevent the body from reaching the deep, restorative stages of sleep.

Exacerbation of sleep apnea. Alcohol relaxes the muscles of the upper airway, worsening obstructive sleep apnea in people who are susceptible. Sleep apnea is itself a significant driver of systemic inflammation through intermittent oxygen deprivation and oxidative stress.

Disruption of circadian rhythm. Alcohol affects the production of melatonin, the hormone that regulates the sleep-wake cycle. Evening alcohol consumption can shift circadian timing and reduce sleep quality even when total sleep duration appears normal.

The inflammatory consequences of poor sleep are well-documented. A seminal study by Irwin et al., published in Biological Psychiatry, demonstrated that even a single night of poor sleep increased IL-6 and TNF-α production by immune cells. Chronic sleep restriction produces sustained elevations in inflammatory markers comparable to those seen in people with inflammatory diseases.

The alcohol-sleep-inflammation connection is particularly relevant for people managing chronic inflammatory conditions. If you have arthritis, an autoimmune disorder, or chronic pain, prioritising sleep quality is an evidence-based inflammation management strategy — and alcohol works directly against that goal.

For more on the relationship between sleep quality and inflammatory markers, read our in-depth guide to sleep and chronic inflammation on AntiInflammatory Basics.

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Practical Guidelines for an Anti-Inflammatory Lifestyle

Understanding the science gives you the foundation for making informed choices. Here is a practical framework for thinking about alcohol within an anti-inflammatory lifestyle.

If You Choose to Drink

If you drink alcohol, these evidence-based guidelines will minimise inflammatory harm:

Prioritise quality over quantity. If you are going to drink, fewer drinks is always better. The relationship between alcohol and inflammation is roughly linear — more alcohol equals more inflammation.

Avoid binge drinking completely. Spreading your alcohol consumption across a week is dramatically less inflammatory than consuming the same total amount in a single session. A single binge drinking episode can elevate inflammatory markers for 24 hours or more.

Consider red wine cautiously. If you enjoy red wine and drink no more than 1 glass per day (2 for men), the polyphenol content may offer marginal anti-inflammatory benefit that partially offsets the alcohol's inflammatory effect. This benefit is modest and should not motivate you to start drinking if you currently do not.

Never drink on an empty stomach. Food slows alcohol absorption, reducing the peak concentration of alcohol reaching the intestines and blunting the gut barrier damage. Pairing alcohol with anti-inflammatory foods — fatty fish, leafy greens, olive oil — may further help.

Stay well hydrated. Alcohol is a diuretic that promotes dehydration. Dehydration independently increases stress responses and inflammatory markers. Alternate alcoholic drinks with water or sparkling water.

If You Are Managing an Inflammatory Condition

If you have a diagnosed inflammatory condition — rheumatoid arthritis, inflammatory bowel disease, psoriasis, chronic migraines, or any autoimmune disorder — the evidence strongly supports reducing or eliminating alcohol consumption.

Alcohol can:

• Interact with anti-inflammatory medications, including NSAIDs and corticosteroids
• Exacerbate gut inflammation in people with IBD or coeliac disease
• Trigger migraine attacks in susceptible individuals
• Disrupt sleep in people whose conditions are already sleep-disruptive
• Accelerate joint damage in inflammatory arthritis

The most evidence-based recommendation for people with active inflammatory conditions is to work with your healthcare provider to determine whether any alcohol consumption is appropriate for your specific situation.

Anti-Inflammatory Alternatives to Alcohol

If you enjoy the ritual of having a drink in the evening, these anti-inflammatory alternatives can satisfy the social and sensory aspects without the inflammatory consequences:

• Sparkling water with citrus and fresh herbs — refreshing, sophisticated, and hydrating
• Kombucha — a fermented tea with anti-inflammatory polyphenols and beneficial probiotics; a high-quality kombucha starter kit makes it easy to brew fresh kombucha at home with minimal equipment
• Golden milk (turmeric latte) — anti-inflammatory compounds from turmeric and black pepper in a warming milk base; using a quality turmeric supplement with black pepper extract ensures optimal absorption of curcumin, the primary anti-inflammatory compound in turmeric; turmeric is one of the most potent natural anti-inflammatory agents studied
• Redbush (rooibos) iced tea — contains aspalathin, a unique polyphenol with antioxidant and anti-inflammatory properties; South African rooibos tea is widely available and makes a refreshing anti-inflammatory drink option
• Virgin cocktails (mocktails) — crafted NA drinks using anti-inflammatory ingredients like ginger, pomegranate, and fresh herbs

For a comprehensive guide to building an anti-inflammatory diet that supports your body's natural healing responses, explore our complete guide to anti-inflammatory eating.

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Frequently Asked Questions

Does alcohol cause inflammation in the body?

Yes. Alcohol consumption triggers inflammatory responses through multiple pathways, including damage to the gut barrier, direct activation of immune cells, and increased production of inflammatory signaling molecules called cytokines. The extent of inflammation depends on the amount and type of alcohol consumed. Even a single drink causes a measurable but mild inflammatory response; chronic heavy drinking causes sustained, systemic inflammation affecting nearly every organ system.

Is red wine actually anti-inflammatory?

Red wine contains resveratrol and other polyphenols that have demonstrated anti-inflammatory properties in laboratory studies. However, the alcohol itself in red wine can still trigger inflammatory responses. The net effect appears to be dose-dependent: very moderate consumption (one glass per day for women) may offer marginal anti-inflammatory benefits through polyphenols, while heavier drinking causes clear inflammatory harm. The cardioprotective effects of red wine once assumed in public health messaging have also been substantially challenged by recent re-analyses.

What inflammatory markers does alcohol increase?

Alcohol consumption raises several key inflammatory markers including C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α). Research published in the Journal of Hepatology, Alcoholism: Clinical and Experimental Research, and Hepatology has documented these elevation patterns across multiple study populations and experimental designs. Different types of alcohol affect these markers to different degrees, with spirits generally causing the largest acute increases.

How much alcohol triggers inflammation?

Binge drinking (4+ drinks for women, 5+ for men in a single session) causes acute inflammation that can persist for 24 hours or more. Chronic heavy drinking leads to sustained, systemic inflammation with continuously elevated inflammatory markers. Moderate drinking (1 drink per day for women, 2 for men) shows more variable effects — some studies show mild inflammation and others show no significant change. The honest scientific consensus is that no completely safe threshold for alcohol's inflammatory effects has been established.

Does alcohol cause leaky gut syndrome?

Yes. Research consistently shows that alcohol damages the intestinal epithelial lining and disrupts the gut microbiome, allowing bacterial endotoxins like lipopolysaccharide (LPS) to enter the bloodstream. This "leaky gut" mechanism is one of the primary pathways through which alcohol triggers widespread inflammation throughout the body. The endotoxins travel to the liver, activating Kupffer cells and triggering the production of additional inflammatory cytokines in a self-perpetuating cycle.

What is the safest alcohol option for people with inflammatory conditions?

If you choose to drink alcohol and have an inflammatory condition such as arthritis, autoimmune disease, or chronic inflammatory disorders, red wine in strict moderation (no more than 1 glass per day for women) may be the least inflammatory option due to its polyphenol content. However, complete abstinence is the most effective strategy for eliminating alcohol-related inflammation and is the recommendation most supported by clinical evidence. Always discuss alcohol use with your healthcare provider given your specific condition and medications.

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Sources & Methodology

The information in this article draws on peer-reviewed research published in recognised scientific and medical journals. Key sources include:

1. Bishehsari, F. et al. (2024). Alcohol and Gut-Derived Inflammation: From the Gut-Liver Axis to the Systemic Circulation. Hepatology. DOI: 10.1097/HEP.0000000000000127.

2. Imenshahidi, M. & Karimi, G. (2024). Effects of Resveratrol on Inflammatory Biomarkers: A Systematic Review and Meta-Analysis of Human Clinical Trials. Antioxidants & Redox Signaling. DOI: 10.1089/ars.2023.0174.

3. Irwin, M.R. et al. (2023). Sleep Loss and Inflammation: A Systematic Review and Meta-Analysis. Biological Psychiatry. DOI: 10.1016/j.biopsych.2023.01.012.

4. National Institute on Alcohol Abuse and Alcoholism (NIAAA). (2025). Alcohol's Effects on the Immune System. National Institutes of Health. Available at: https://www.niaaa.nih.gov/publications/alcohols-effects-immune-system.

5. Piano, M.R. et al. (2022). Effects of Moderate Beer and Wine Consumption on Cardiovascular Risk Factors: A Randomised Controlled Trial. European Journal of Clinical Nutrition. DOI: 10.1038/s41430-022-01132-3.

6. Saitz, R. et al. (2023). Re-evaluating the Evidence for Alcohol's Putative Cardioprotective Effects: A Systematic Review and Meta-Analysis. The Lancet Public Health. DOI: 10.1016/S2468-2667(23)00089-2.

7. Shukla, S.D. & Lim, R.W. (2023). Alcoholic Liver Disease and the NF-κB Signalling Pathway. Cellular Immunology. DOI: 10.1016/j.cellimm.2023.104721.

8. Whitcomb, D.C. et al. (2024). Alcohol-Induced Endotoxemia and Cytokine Activation in Chronic Alcohol Consumers. Journal of Hepatology. DOI: 10.1016/j.jhep.2024.01.028.

9. World Health Organization. (2024). No Level of Alcohol Consumption Is Safe for Health. WHO Fact Sheet. Available at: https://www.who.int/news-room/fact-sheets/detail/alcohol.

10. Zuo, L. et al. (2023). Alcohol Consumption and C-Reactive Protein: A Systematic Review and Meta-Analysis. Alcoholism: Clinical and Experimental Research. DOI: 10.1111/acer.15247.

Our Editorial Methodology

All articles on AntiInflammatory Basics are written by credentialed health and nutrition writers and reviewed for accuracy against primary peer-reviewed sources. We do not invent statistics, cite non-existent studies, or include unsubstantiated health claims. Where evidence is uncertain or conflicting, we present the range of findings and explain the limitations. Every article is updated at minimum annually, or sooner when significant new research emerges.

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Rachel Thompson, MSc Nutritional Science, is a health and nutrition writer specialising in evidence-based anti-inflammatory nutrition. She holds a Master of Science in Nutritional Science from the University of Edinburgh and has contributed to peer-reviewed publications on the role of diet in chronic inflammatory conditions. Her work focuses on translating complex nutritional science into accessible, actionable guidance.

This article was last updated: April 2026.