Alcohol Consumption Behaviors and Liver Disease: Is There a Safer Drinking Practices?

Introduction

Alcohol-associated liver disease (ALD) is a progressive spectrum of liver disorders caused by chronic excessive alcohol use, ranging from alcohol-associated fatty liver disease to cirrhosis and hepatocellular carcinoma. With the global decline in viral hepatitis, due to improved antiviral therapies, the proportion of liver diseases attributable to alcohol has increased substantially. ALD now represents one of the leading causes of liver-related morbidity and mortality worldwide [1]. Compared with patients with liver diseases of other etiologies, patients with ALD have a faster disease progression and are more likely to seek medical treatment at an advanced stage [2,3]. Li et al found that alcoholic cirrhosis presents a higher risk of decompensation-related mortality than does virally-induced cirrhosis, with a risk ratio of 1.20 [4].

Globally, approximately 2.348 billion people consume alcohol, with an average annual pure alcohol consumption of 6.4 L per person, equivalent to a daily intake of 13.9 g [5]. Alcohol consumption is a major contributor to cirrhosis, accounting for nearly 60% of cases in Europe, North America, and Latin America [6]. Nasr et al analyzed liver disease in Sweden from 2005 to 2019 and found that the incidence of ALD increased by 47% and was the highest incidence of liver disease in 2019 (age-standardized mortality rate of 16.4) [7].

The global burden of ALD continues to rise despite decades of research on total alcohol intake thresholds. This paradox underscores a critical gap: clinicians lack actionable guidance for modifying drinking behaviors linked to ALD progression. Current guidelines emphasize abstinence or dose reduction [8] yet fail to consider the nuanced risks associated with how individuals drink. Therefore, in this review, we aim to identify healthier drinking patterns, through a comprehensive literature review, with the goal of providing insights to help mitigate the burden of ALD. We performed a PubMed database search from inception to February 2025 using English-language articles and the following keywords: “alcohol-associated liver disease”, “alcohol-associated cirrhosis”, “drinking pattern”, “binge drinking”, and “abstinence”.

Drinking Patterns

Existing evidence suggests that the risk and progression of ALD are not solely determined by the total amount of alcohol consumed [9–11]. Instead, specific drinking behaviors – how, when, and what people drink – can modify the extent of liver damage. In contrast to the non-modifiable factors, such as sex, age, and genetics, drinking patterns are modifiable and can be targeted in clinical assessments and public health strategies. However, they are often overlooked despite their critical role in influencing ALD risk and progression. Drinking patterns encompass the behavioral characteristics and habits exhibited by an individual during alcohol consumption. The existing literature primarily discusses drinking patterns in terms of the following aspects: the amount of alcohol consumed, drinking frequency, speed, duration, type of alcoholic beverage, and whether alcohol is consumed with meals [9,12]. Exploring these patterns individually allows for a more nuanced understanding of their unique contributions to ALD development. In this section, we delve into various drinking behaviors that shape the pathogenesis of ALD, providing insights into how each pattern can influence the clinical course and outcomes of the disease. The purpose is to pay more attention to drinking patterns and fully understand their relationship with ALD.

Different Drinking Patterns and ALD

ALCOHOL CONSUMPTION AMOUNT:

The alcohol consumption amount refers mostly to the intake of pure alcohol. The calculation formula of alcohol consumption amount is as follows: alcohol consumption amount (g) = alcohol volume (mL) × alcohol content (%) ×0.8. Some publications and literature differentiate between different levels of alcohol consumption. Moderate drinking is defined as <28 g/day for men and <14 g/day for women, according to the Dietary Guidelines for Americans, 2020–2025 [13]. The National Institute on Alcohol Abuse and Alcoholism defines heavy alcohol use as >56 g/day or 196 g/week for men and >42 g/day or 98 g/week for women [14]. Some studies suggest that drinking 30 g/day for men and 20 g/day for women is a risk threshold for developing ALD and also a reference threshold for differentiating ALD from non-alcoholic fatty liver disease [15–17]. The World Health Organization defines heavy episodic drinking as consuming ≥60 g of alcohol in the same occasion at least once a month [5]. These standardized definitions by some health organizations or institutions aim to help individuals regulate or limit their daily alcohol consumption.

Research suggests a dose-dependent relationship between alcohol intake and the development of liver disease, with higher consumption levels correlating with increased risk. In a large cohort study involving approximately 400 000 women in the United Kingdom, Simpson et al reported that the incidence of cirrhosis rose with increasing alcohol intake. Specifically, women consuming more than 220 g/week had a significantly higher risk than did those consuming 30 g/week (relative risk=3.43) [9]. A cross-sectional study of 1966 participants found that for every additional 10 g/day of alcohol consumed, the risk of fatty liver disease increased by 9% [18].

However, the concept of a threshold effect has emerged, suggesting that once alcohol intake reaches a certain level, the associated risk plateaus and does not significantly escalate with further consumption. Research conducted by Kamper-Jørgensen et al, involving 6152 individuals with alcohol use disorder, identified 60 g/day as the threshold for cirrhosis-related mortality[19]. Beyond this level, increased consumption did not further heighten the risk of death, supporting the notion of a threshold effect on mortality risk. Additionally, Wang et al found that in patients with ALD and pre-existing liver function impairment, large quantities of alcohol intake did not exacerbate their liver condition, further corroborating the threshold effect hypothesis [20]. According to the studies by Hagström et al, when alcohol consumption is less than 60 g/day, the risk of developing severe liver disease increases by 1.7% for each additional 1 g/day of alcohol intake. The highest risk is observed at a consumption level of 60 g/day, at which point the risk is 3.66 times that of non-drinkers [21]. This suggests a dose-dependent hepatotoxic effect of alcohol at lower intake levels, shifting to a threshold effect at higher consumption.

Some studies are controversial regarding the effects of low alcohol consumption on the liver. Xue et al found that men who consumed less than 30 g/day and women who consumed less than 20 g/day had a 23% lower risk of developing severe liver disease than non-drinkers [22]. Results of a meta-analysis showed that low alcohol consumption (0–14.9 g/day) can decrease the risk of liver cancer by 27% [23]. However, other sensitive factors, such as sex and geography, were not analyzed. The applicability of the results to different types of populations remains inconclusive. Conversely, other studies have found that even small amounts of alcohol can cause liver damage. Louvet et al found that in patients with alcoholic cirrhosis, drinking 10 to 60 g/week was associated with an increased risk of death (hazard ratio [HR]=1.49) and liver complications (HR=1.67) [24]. Aberg et al observed that alcohol intake of 0 to 9 g/day was associated with a non-significant increase in liver disease risk, compared with not drinking, while intake of 10 to 19 g/day was significantly associated with more than a 2-fold increase in risk [25].

The control of alcohol consumption plays a crucial role in maintaining liver health. Although guidelines have been established to define moderate and heavy drinking based on different levels of alcohol intake, there are significant individual differences in response to alcohol, making it challenging to apply uniform recommendations to everyone. Moreover, the effects of low-level alcohol consumption remain to be further studied. Therefore, we do not recommend that individuals who do not drink start drinking, even in small amounts. For those who do drink, we advise them to abstain from alcohol or reduce their alcohol intake as much as possible.

DRINKING SPEED:

The speed of alcohol consumption significantly impacts liver health. The pattern of consuming a large amount of alcohol within a short period is referred to as binge drinking. According to the National Institute on Alcohol Abuse and Alcoholism, binge drinking is defined as drinking ≥70 g of alcohol in 2 h for men and ≥56 g for women, with a total blood alcohol concentration of 0.08 g/dL or higher [14].

An epidemiological study has shown a trend toward younger onset of ALD in the United States between 1999 and 2018, with mortality rates in 25 to 34 year olds with ALD increasing faster than in older individuals [26]. This trend may be attributed to a rise in binge and heavy drinking among younger populations, compared with previous generations. Ding et al found that increased alcohol consumption during binge drinking is associated with an increased risk of liver disease. Compared with women consuming less than 24 g/day and men consuming less than 32 g/day, binge drinkers had a 1.37-fold higher risk of alcoholic cirrhosis and a 4.16-fold higher risk of alcoholic hepatitis. Among heavy binge drinkers (≥72 g/day for women and ≥96 g/day for men), the risk was even greater, with increases ranging from 2.85- to 8.38-fold [27].

To mitigate the adverse effects of binge drinking, it is critical to promote slower drinking habits and discourage excessive alcohol consumption in a single sitting. Moderating the pace of alcohol consumption can help mitigate the detrimental effects of alcohol on the liver.

DRINKING FREQUENCY:

Drinking frequency refers to the number of times or days of drinking over a period of time. Most studies have used the number of days per week as the frequency of drinking. In Japan, the term “liver holiday” is popular, which means that abstaining from alcohol for 2 or more days per week is important for maintaining health and liver metabolism [28]. Individuals who drink daily are continuously exposed to the acetaldehyde produced by alcohol metabolism, which increases the harmful effects of acetaldehyde on the liver, compared with those who take a “liver holiday” [28]. Consistent with this, other research supports the idea that reducing drinking frequency, even when consuming the same total amount of alcohol, results in less liver damage.

For example, a cohort study by Askgaard et al revealed that, in men, daily drinking was associated with a 2.65-fold higher risk of cirrhosis than was consuming alcohol 2 to 4 days per week. In women, daily drinking increased the risk by 73% [12]. Simpson et al demonstrated a 61% higher cirrhosis risk with daily drinking than in infrequent drinking [9]. A meta-analysis showed that compared with non-daily drinking, daily drinking was associated with a significantly increased risk of cirrhosis, with a combined relative risk of 1.71 for men and 1.56 for women [11].

However, it remains unclear whether similar outcomes apply to higher levels of alcohol consumption, as individuals who drink frequently tend to consume more alcohol overall. Nonetheless, adopting “liver holidays” could be a practical and effective strategy for mitigating liver damage, as it allows the liver time to recover from alcohol-related stress. Encouraging individuals to decrease the frequency of alcohol consumption could be an effective strategy to lower the incidence of cirrhosis and enhance liver health.

DURATION OF DRINKING:

The duration of drinking refers to the length of time an individual has consumed alcohol, typically measured from the onset of regular drinking to the present, or the point of abstinence. Long-term alcohol consumption is a well-established risk factor for ALD, with significant associations observed even at moderate daily intake levels [30]. Epidemiological evidence indicates that sustained intake above 30 g/day for women or 50 g/day for men for over 5 years markedly elevates alcohol-associated cirrhosis risk [31].

A study conducted by Kakunje et al found that patients with alcoholic cirrhosis had a significantly longer drinking history (22.6±7.65 years) than those with alcohol dependence alone (19.3±6.95 years) [32]. Similarly, Corrao et al observed that the risk of developing cirrhosis was highest after 10 to 20 years of drinking, with no evidence of reduced risk associated with longer durations of alcohol consumption [33]. However, the potential influence of survivorship bias cannot be excluded.

The cumulative effects of prolonged alcohol exposure highlight the importance of timely interventions to reduce drinking duration. However, individuals with persistent drinking tend to drink for longer periods of time, which seems uncontrollable. Therefore, providing good health education in a timely manner may effectively encourage individuals who drink to quit drinking as early as possible, thereby shortening the duration of drinking and reducing related health risks.

TYPE OF ALCOHOLIC BEVERAGE:

Alcoholic beverages are categorized into fermented alcohol (eg, beer, wine) and distilled liquor (eg, spirits, tequila). Research suggests that the type of alcohol consumed can significantly influence the risk of ALD, with distilled liquors generally posing a greater risk than fermented beverages due to their higher alcohol concentration and typical consumption patterns. Tverdal et al found that the risk of death from ALD varied among patients who drank different types of alcoholic beverages, including beer (HR=2.06), wine (HR=0.68), and liquor (HR=2.54) [10]. Similarly, Minea et al found that excessive consumption of distilled spirits in men was more than twice as likely to lead to advanced liver fibrosis (odds ratio [OR]=6.43) than was wine consumption (OR=2.04) [34]. Becker et al found that, compared with individuals who did not drink wine, the relative risk of developing cirrhosis was 0.4 for those who drank 16% to 30% of their total alcohol intake as wine, and the relative risk of developing cirrhosis was 0.3 for those who drank 51% or more of their total alcohol intake as wine [35]. However, these studies did not entirely exclude the potential influence of confounding variables, such as relatively healthy drinking patterns (eg, lower alcohol consumption per session) and lifestyle (eg, good dietary habits). Consequently, the observed differences in the risk of liver disease among individuals consuming different types of alcoholic beverages may partly stem from these underlying factors.

People with alcoholic cirrhosis seem to drink more distilled alcohol. A study from Mexico analyzed the drinking patterns in 124 patients with cirrhosis and found that their most commonly consumed alcoholic beverage was tequila, a distilled liquor made from agave that is processed through distillation [36]. A study from the United States analyzed the association between distilled liquor and the prevalence of cirrhosis between 1949 and 1994, and found that, among all alcoholic beverages, the consumption of distilled liquor was most strongly associated with mortality from cirrhosis [37]. Other studies have suggested that the alcohol consumption when drinking distilled liquor is usually more than twice that of other alcoholic beverages [20]. Consequently, the increased risk of cirrhosis among distilled spirit consumers may be attributed to their higher levels of alcohol intake.

Some studies suggest that drinking wine in small amounts can even have a protective effect on the liver. This may be due to the bioactive components of wine, such as polyphenols, including anthocyanins, resveratrol, and gallic acid, which have antioxidant, lipid metabolism-regulating, microbial population-regulating, ethanol-induced oxidative stress-reducing, and anticancer effects [38,39]. Liu et al found that men who consumed less than 30 g/day of wine and women who consumed less than 20 g/day of wine exhibited lower levels of alanine aminotransferase and aspartate aminotransferase than did non-drinkers [40]. Alcohol consumption within this range was also linked to a reduced risk of liver fibrosis, cirrhosis, and hepatocellular carcinoma [40]. Furthermore, Askgaard et al found that consuming wine was associated with a relatively low risk of developing alcoholic cirrhosis when alcohol intake was kept below 28 to 35 drinks per week (12 g per drink) and wine made up little of the overall amount [12]. However, at higher consumption levels, this protective effect was not observed, suggesting that the hepatoprotective effects of wine can be confined to specific intake thresholds.

Although moderate wine consumption appears to have potential benefits, further research is required to clarify the biochemical mechanisms underlying these effects and to distinguish between the impacts of alcohol type and drinking patterns. For those unable to abstain completely, substituting distilled liquors with fermented beverages, particularly wine, may help reduce ALD risk. However, public health guidelines should emphasize the importance of overall alcohol reduction, regardless of the type of beverage.

ALCOHOL CONSUMPTION WITH MEALS:

The context in which alcohol is consumed, such as whether it is taken with or without meals, significantly influences the impact on liver health. Studies suggest that drinking alcohol with meals produces less liver damage than consuming alcohol on an empty stomach. Bellentani et al concluded that individuals with non-mealtime drinking were 3.4 to 5.0 times more likely to develop ALD or progress to cirrhosis than those who drank with a meal [15]. Simpson et al similarly observed a 20% elevated cirrhosis risk in individuals with non-mealtime drinking, after controlling for total alcohol consumption, body mass index, and smoking status [9]. The protective effect of drinking with meals may be attributed to the reduced peak blood alcohol concentration achieved when food is present in the stomach. This physiological buffering effect mitigates oxidative stress and may decrease the cumulative risk of alcohol-related hepatic damage [41].

Compared with drinking on an empty stomach, drinking during or after a meal can reduce the damage of alcohol to the liver. The findings could help people reduce their risk of liver disease by adjusting their drinking and eating habits. Further research is needed to explore cultural variations and individual differences in meal composition and timing, which can influence these outcomes.

Abstinence and ALD

Alcohol abstinence is considered the most effective strategy to halt the progression of ALD at any stage and improve long-term prognosis [8]. Abstinence from alcohol is an important factor in predicting the prognosis of patients with ALD and can improve the survival rate of patients [42]. Studies have shown that abstaining from alcohol can improve liver lipid metabolism, reverse some liver damage and inflammation, and improve complications caused by cirrhosis, such as portal hypertension [30,43]. A prospective study by Hofer et al involving 320 patients with alcoholic cirrhosis showed that alcohol abstinence not only improved portal hypertension but also reduced liver-related mortality by 57.2% [44]. A meta-analysis covering 19 studies conducted by Lim et al showed that abstinence from alcohol was significantly associated with improved overall survival in patients with alcoholic cirrhosis [45]. Those who did not abstain had an overall survival rate that was approximately 39% lower than those who abstained from alcohol.

While reducing alcohol consumption may confer some protective effects, these findings consistently underscore that complete abstinence remains the criterion standard in ALD prevention and management. Healthcare providers should prioritize interventions that support and encourage abstinence, acknowledging both the immediate and long-term health benefits.

Conclusions

This review synthesizes evidence that drinking patterns modulate the risk and progression of ALD. Lower alcohol consumption, slower drinking speed, lower frequency of drinking, shorter cumulative drinking histories, substitution of distilled spirits with fermented beverages, and consuming alcohol with meals emerged as practicable harm-reduction strategies, particularly for individuals unable to achieve full abstinence. From a public health perspective, promoting these modified behaviors may help lower ALD incidence in populations in which abstinence is not attainable. However, it is important to emphasize that abstinence remains the most effective measure for preventing and managing ALD at all stages. Future research should clarify biological mechanisms linking specific drinking behaviors to hepatotoxicity and evaluate long-term outcomes of pattern-targeted interventions to inform global public health strategies.