Publications > Journals > Journal of Clinical and Translational Hepatology > Article Full Text


Alcohol and Metabolic-associated Fatty Liver Disease

  • Fu-Rong Sun and
  • Bing-Yuan Wang* 
 Author information
Journal of Clinical and Translational Hepatology 2021;():-

DOI: 10.14218/JCTH.2021.00173


The diagnosis of metabolic-associated fatty liver disease is based on the detection of liver steatosis together with the presence of metabolic dysfunction. According to this new definition, the diagnosis of metabolic-associated fatty liver disease is independent of the amount of alcohol consumed. Actually, alcohol and its metabolites have various effects on metabolic-associated abnormalities during the process of alcohol metabolism. Studies have shown improved metabolic function in light to moderate alcohol drinkers. There are several studies focusing on the role of light to moderate alcohol intake on metabolic dysfunction. However, the results from studies are diverse, and the conclusions are often controversial. This review systematically discusses the effects of alcohol consumption, focusing on light to moderate alcohol consumption, obesity, lipid and glucose metabolism, and blood pressure.


Alcohol, Metabolic-associated fatty liver disease, Obesity, Insulin resistance, Hypertension


In 2020, the definition of metabolic-associated fatty liver disease (MAFLD) was proposed by Eslam et al.1 Since then, clinical practice guidelines on MAFLD have been published by the Asian Pacific Association for the Study of the Liver.2 An important significance of this definition is the “positive” criteria for the diagnosis of MAFLD, in contrast to a diagnosis of exclusion. More importantly, it is possible to diagnose MAFLD coexisting with liver injury caused by other reasons. The diagnosis of MAFLD is based on the detection of liver steatosis together with the presence of metabolic dysfunction, such as overweight or obesity, type 2 diabetes mellitus (T2DM), or clinical evidence of metabolic risk abnormalities.1 The absence of alcohol intake limit is the prominent difference between the diagnostic criteria of MAFLD and the previous diagnostic criteria of non-alcoholic fatty liver disease. As is well known, a lack of ongoing or current consumption of significant amounts of alcohol was an important indicator in the latter.3 However, the diagnosis of MAFLD is independent of the amount of alcohol consumed. Thus, it is possible to diagnose MAFLD coexisting with alcoholic-related liver disease (ALD).

Alcohol consumption is common in the general population. There are several common drinking patterns, including chronic heavy drinking,4 light alcohol consumption, moderate alcohol consumption (MAC),4,5 and binge drinking (Table 1). It has been well accepted that chronic heavy drinking is related with high risk of ALD and should be avoided. Compared with the chronic heavy drinking population, the non-heavy drinking population is much larger. Binge drinking, which is often related with serious social problems and deteriorative health problems, is another popular drinking pattern nowadays, especially among young people. Binge drinking could happen monthly or weekly, but it is different from chronic regular heavy drinking. The prevalence of binge drinking has significantly increased over the past two decades, with an average annual increase of 0.72% per year.6 Binge drinking can coexist with MAC or regular heavy drinking, inducing antagonistic or synergistic effects.

Table 1

Drinking patterns in this review

Drinking patternDefinition
Chronic heavy drinkingChronic alcohol consumption (generally more than 5 years) more than 60 g on one occasion4
Binge drinkingAlcohol consumption >40 g for women and >50 g for men within about 2 h1
Non-heavy drinkingMACRegular alcohol drinking <30-42 g/day for men and <20-28 g/day for women4,5
Light alcohol consumptionRegular alcohol drinking <10-20 g/day for most studies

Alcohol consumption and metabolic dysfunction are two main causes of chronic liver injury and can interact with each other. Early studies showed that MAC might be associated with improved dyslipidemia and reduced cardiovascular risk, indicating MAC may be related with restored metabolism. Several studies were conducted to investigate the role of light to moderate alcohol consumption (LMAC) in metabolic disorders. It has been demonstrated that alcohol and its metabolites have multiple effects on metabolic-associated factors, such as body weight, glucose and lipid metabolism, and the cardiovascular system. However, there is still no consensus on the effects of alcohol on metabolic-related diseases. At the same time, the above-mentioned metabolic abnormalities are the focus of MAFLD. This review systematically discusses the effects of alcohol consumption on obesity, lipid and glucose metabolism, and blood pressure, focusing on the effects of non-heavy alcohol consumption, to help better understand the relationship between alcohol consumption and MAFLD.

Alcohol consumption and overweight/obesity

Effects of alcohol consumption on body weight

There is a higher risk of overweight/obesity in chronic heavy drinkers, mainly showing as higher body mass index (BMI) and increased waist circumference (WC).7,8 A previous study showed a 17% higher risk for WC gain in men consuming 1,000 mL/day beer compared with those drinking less than 250 mL/day beer.9 There seems to be a stronger connection between heavy drinking and increased body weight in men at different ages than in women.8,10 In elderly men, greater BMI (+4.8%) and WC (+5%) were shown to be related to alcohol intake ≥50 g/day.8 Energy from alcohol metabolism (7.1 kcal generated by 1 g ethanol) accounts for the increased total energy intake in heavy drinkers, partly contributing to increased body weight and BMI. Studies showed that alcohol intake of more than 3–5 drinks/day can dramatically increase the energy intake from alcohol.7,8 More importantly, chronic heavy drinking has been proven to induce pancreatic β-cell dysfunction in human and animal models,11,12 with decreased insulin-secretory ability and disrupted glucose homeostasis. Both increased energy intake and pancreatic β-cell dysfunction contribute to the pathogenesis of obesity in heavy drinkers. Heavy drinking-associated pancreatic β-cell dysfunction may play a more crucial role than increased energy intake in the development of MAFLD.

The effects of occasional binge drinking on body weight may be not obvious in the short term. However, frequent binge drinking could significantly increase the risk of becoming overweight and obese13 and the risk of abdominal obesity in men.14 On the one hand, frequent binge drinking has a similar effect as chronic heavy drinking as it involves increased energy intake. On the other hand, binge drinking could induce systemic insulin resistance (IR) by impairing hypothalamic insulin action, manifesting as suppressed hepatic glucose production and white adipose tissue lipolysis.15 Besides, binge drinking is often accompanied by increased high-fat food intake and even binge eating,16 indicating a much higher energy intake, thereby increasing the body weight. As a result, the increased energy intake and the glucose and lipid metabolism abnormalities induced by impaired insulin signaling eventually lead to increased body weight.

Clinical studies have shown that moderate drinking may help maintain normal weight and is associated with a lower prevalence of obesity than in non-drinkers,17,18 showing as lower BMI values (by 1.34 kg/m2),19 a lower total abdominal fat volume, and less subcutaneous adipose tissue.20 Among normal-weight middle-aged and older women, LMAC is associated with smaller weight gain and a lower risk of becoming overweight and/or obese compared to non-drinkers.21 Similarly, LMAC does not increase the risk of increase in the BMI and WC in elderly men.8 Moderate wine consumption (150 mL/day), as part of a Mediterranean diet, in persons with controlled diabetes does not promote weight gain or abdominal adiposity.22 These results indicate a potentially beneficial effect of moderate drinking on maintaining a normal body weight in different populations, a different effect from that of heavy or binge drinking.

LMAC could regulate body weight through several mechanisms. Alcohol tends to increase appetite and food intake, probably through short-time reward effects of food and through the regulation of the expression of various neurotransmitters,23,24 leading to increased total energy intake. However, the energy obtained from alcohol becomes part of the total daily energy intake in the long term; accordingly, the energy intake, excluding the calories from alcohol, decreases.21 The reward effects of food gradually weaken and are even offset due to the reduction in total food intake or carbohydrate/fat intake.23 Therefore, body weight probably does not increase significantly in chronic regular drinkers. Besides, MAC could decrease the body weight by improving IR, an opposite effect compared with heavy or binge drinking, showing as decreased body weight, decreased liver weight and triglyceride (TG) levels, and reduced glycemia and insulinemia in animal models.25 Hence, LMAC drinkers tend to avoid significant body weight gain, in contrast to heavy drinkers.26 Changes in body weight could be the result of an imbalance between (i) the regulation of the central nervous system and peripheral insulin function and (ii) energy use. However, the exact underlying mechanisms remain unclear, and more studies are required.

Combined effects of overweight/obesity and alcohol on liver

Heavy and binge drinking are often associated with high risk of fatty liver disease. Overweight/obesity can further promote the development of fatty liver disease.27,28 Long-term obesity (longer than 10 years), especially abdominal obesity, is an important risk factor for alcoholic-related liver cirrhosis and alcoholic hepatitis29,30 and is associated with an increased risk of 3-month mortality in alcoholic hepatitis (hazard ratio [HR]: 2.22, 95% confidence interval [CI]: 1.1–4.3).31 A binge-like drinking pattern is independently associated with significant liver fibrosis progression in overweight/obese patients with MAFLD.28 These results demonstrate that there are synergistic effects of high alcohol intake and of being overweight/obese on liver injury and an increased risk of fatty liver disease.

LMAC seems to play different roles in fatty liver disease. Studies showed that LMAC reduces the risk of fatty liver disease by 22.6% in general population,32,33 and it reduces the risk of fatty liver disease by 31.3% in overweight and obese people.33 Mild liver inflammation and fibrosis with a low risk of advanced liver fibrosis (stage F3/F4) were found in obese patients with MAC, compared with non-drinkers.3437 Our previous studies also showed that chronic MAC is related with alleviated liver fibrosis in a high-fat and high-cholesterol diet-induced liver fibrosis model, probably via reduced activation of Kupffer cells and hepatic stellate cells.38 However, an increased risk of advanced liver cirrhosis in LMAC has been reported. A recent Asian population study showed that MAC reduced the risk of hepatic steatosis in overweight/obese individuals, while MAC increased the risk of advanced liver fibrosis (HR: 1.49, 95% CI: 1.33–1.66), as estimated by the fibrosis-4 index in overweight or obese individuals after a 15.7-year follow-up.39 In another cross-sectional study among obese patients with T2DM, LMAC was found to be associated with an increased probability of advanced fibrosis in biopsy-proven MAFLD (odds ratio [OR]: 5.5–9.7, 95% CI: 1.05–69.6).40 So far, the long-term impacts of LMAC on liver cirrhosis among obese people are still uncertain. More histological evidence is urgently needed to verify the role of LMAC in liver cirrhosis among obese people.

Adipose tissue can serve as another important source of proinflammatory factors that contribute to liver injury. Proteome analysis of serum inflammatory factors showed higher expression of chemokines (C-X-C motif and C-C motif ligands), interleukins (ILs), and tumor necrosis factor-alpha (TNF-α) in obese individuals than in non-obese controls; for example, CXCL 11 was markedly upregulated (by 40%) in obese patients and in adipose tissue in a murine model.31 In adipose tissue, adipocytes can recruit immune cells (such as macrophages, neutrophils, and lymphocytes) and polarize them to their proinflammatory phenotypes to increase the production of proinflammatory cytokines, such as IL-1β, IL-6, IL-12, and TNF-α, and chemokines, promoting tissue inflammation. Macrophages of the proinflammatory M1 phenotype can induce adipocyte death, increasing the release of inflammatory mediators from adipocytes into the extracellular environment, which could recruit and polarize more macrophages.41 In obese people, especially those with abdominal obesity, large amounts of subcutaneous adipose tissue and visceral fat could be important sources of inflammatory factors, which may enhance the effects of heavy drinking on the liver, leading to aggravated liver inflammation.

Cytochrome P450 (CYP) 2E1 is an important enzyme involved in many metabolic processes (including alcohol metabolism). CYP2E1 expression could be induced by alcohol, a high-fat or fructose diet, obesity, and drugs. Excessive CYP2E1 expression is associated with liver inflammation via intrahepatic and extrahepatic mechanisms. Elevated hepatic CYP2E1 mediates endoplasmic reticulum stress and oxidative stress in mitochondria, which contributes to the pathogenesis of ALD and MAFLD.42 In the gut, CYP2E1-mediated oxidative and nitrative stress is related with gut leakiness and endotoxemia, contributing to liver lipid accumulation, increased proinflammatory cytokine production, and infiltration of macrophages in the liver.43 In addition, CYP2E1-induced apoptosis under the coexistence of obesity and binge drinking is involved in liver injury.44,45 Occasional or short-time binge drinking-induced liver injury could probably be restored by compensatory liver function. However, chronic frequent binge drinking or heavy drinking is not favorable for the recovery of the liver. Moreover, repeated inflammatory stimulation of the liver promotes the progression of liver fibrosis.46 Meanwhile, binge eating and high fat intake during binge drinking lead to an increased fat accumulation in the adipose tissue, contributing to the secretion of proinflammatory factors.

Taken together, obesity- and alcohol-induced liver inflammation and fibrosis progression are probably related with interactions among the adipose tissue, the gut, and the liver. Heavy and binge drinking can result in the secretion of more inflammatory factors, contributing to the development of fatty liver disease. The relatively weak proinflammatory effects of LMAC, together with the potential role of LMAC in relieving IR, reduce the risk of fatty liver disease. However, in patients with long-term obesity or T2DM, the protective effects of LMAC may be overshadowed by the increased risk of liver fibrosis or cirrhosis.

Alcohol and lipid metabolism

Elevated plasma TG and decreased high-density lipoprotein (HDL)-cholesterol levels are two important indicators for the diagnosis of MAFLD. The liver is the main organ for both lipid and alcohol metabolism. Increased serum and hepatic TG concentrations are common in alcohol-drinking individuals and animals, including LMAC.4751 TG levels are significantly elevated in heavy drinkers compared with other drinkers and non-drinkers.48 Similarly, binge drinking is associated with a significantly increased risk of elevated TG levels.52 Binge drinking with a high-fat diet or chronic alcohol consumption can synergistically increase peripheral TG levels.53,54 Mechanistic target of rapamycin (mTOR) signaling is considered to play fundamental roles in regulating lipid biosynthesis and metabolism in response to nutrition, showing as mTOR complex 1 (mTORC1) induced lipogenesis through its effect on sterol regulatory element-binding proteins (SREBP), inhibited breakdown of intracellular TG, and reduced fatty acid β-oxidation.55 Recently, studies have demonstrated that mTORC1 is necessary for alcohol to activate hepatic lipogenesis through its effect on SREBP and to inhibit fatty acid β-oxidation, showing as enhanced mTORC1 activity in experimental animals and patients of ALD, characterized by an increase in mTOR-mediated phosphorylation and activity of S6K1, the downstream kinase of mTORC1. Importantly, the concomitant reduction of sirtuin 1 and DEPTOR, an inhibitor of mTOR kinase, signaling was linked to elevated lipogenesis and decreased fatty acid β-oxidation in human liver specimens with ALD. Inhibition of mTORC1 with rapamycin or DEPTOR overexpression ameliorated alcoholic steatosis and liver injury in animals,56 indicating that inhibition of mTORC1 could be a therapeutic target in ALD in the future.

Elevated TG levels are related with alcohol and with enhanced expression levels of enzymes involved in lipid metabolism. During alcohol metabolism, ethanol is first metabolized to acetaldehyde by alcohol dehydrogenase (ADH) and then oxidized to acetic acid by aldehyde dehydrogenase (ALDH). In this process, the consumption of NAD+ is increased and the generation of NADH is increased, resulting in a significant increase in the ratio of NADH:NAD+. The increased ratio further promotes the synthesis of free fatty acids, inhibits fatty acid β-oxidation, and eventually leads to the accumulation of TG in hepatocytes.57,58 Alcohol also upregulates the expression of fatty acid synthase59 and SREBP-1c and downregulates acetyl-CoA carboxylase, the rate-limiting enzyme in fatty acid synthesis, and 5′-AMP-activated protein kinase (AMPK), the central regulator of fatty acid β-oxidation.60,61 A net effect is enhanced fatty acid synthesis, further promoting the synthesis of TG. Long-term heavy alcohol consumption is also related to impaired adiponectin-sirtuin 1-AMPK signaling, a central signaling system controlling the lipid metabolism pathways,62 thereby promoting hepatic steatosis. Therefore, higher amounts of alcohol intake seem more likely to show hepatic steatosis-promoting effects compared with lower amounts of alcohol intake. Besides, insulin is an important hormone involved in lipid metabolism. In the normal state, insulin helps maintain a dynamic balance of lipid metabolism by promoting the export of lipoproteins from the liver and inhibiting lipolysis in adipocytes to facilitate fat storage in adipose tissue.63 Impaired insulin signaling and IR result in decreased serum insulin levels and dysfunction.15,63 Consequently, the effects of insulin in the regulation of free fatty acids are attenuated, contributing to enhanced lipolysis in adipocytes and increased peripheral lipid levels.

HDL plays important roles in cholesterol efflux and reverse cholesterol transport. HDL-cholesterol dyslipidemia is considered to be a major independent risk factor for atherosclerotic cardiovascular disease.64 Alcohol is positively related with HDL metabolism, as plasma HDL-cholesterol concentrations are increased in drinkers compared with non-drinkers.6567 Studies have shown elevated HDL-cholesterol levels in MAC, together with increased apoprotein A-I levels (accounting for 70% of the total HDL protein mass), higher paraoxonase activity, and decreased cardiovascular risk due to its enhanced antioxidative properties.6872 The effects of heavy drinking on HDL seem inconsistent. Some studies observed increased HDL-cholesterol levels and enhanced cholesterol efflux potential in heavy drinkers,66,73 while other studies showed declined HDL levels in patients with alcohol-related fibrosis and cirrhosis.30,74 It is reasonable to assume that the onset of ALD may influence HDL metabolism. However, chronic heavy drinking with or without ALD was associated with a similar declined capacity of cholesterol efflux and reduced cholesterol uptake from peripheral blood in the hepatocytes,74,75 suggesting that alcohol per se is responsible for its deleterious effects on cholesterol efflux and reverse cholesterol transport in heavy drinkers.

Serum HDL levels (quantity) reflect its antioxidant effect to some extent. More importantly, the capacity of cholesterol efflux and reverse cholesterol transport (quality) are two key factors in evaluating its antioxidant capacity. Intact hepatocyte structure and function are necessary for HDL metabolism. During the development of alcohol-related fibrosis and cirrhosis, hepatocytes are gradually depleted, and they become incompetent for lipid metabolism. HDL-cholesterol and total cholesterol levels in peripheral blood are probably not decreased or even increased in the early stage of ALD, partly due to a decline in HDL-mediated reverse cholesterol transport. However, lipid metabolism in the liver gradually weakens with the progression of ALD. Eventually, HDL and total cholesterol levels decrease,76 with declined capacity of cholesterol efflux and reverse cholesterol transport. On the contrary, in LMAC, the liver function is often competent in lipid metabolism; so, higher HDL-cholesterol levels are probably the result of increased synthesis and reverse cholesterol transport, with increased antioxidative properties and capacity of cholesterol efflux, which may prevent lipid deposition in the vessel wall,77 decreasing the risk of cardiovascular disease. However, more studies are needed to confirm these hypotheses.

Alcohol and T2DM

The quantity and function of insulin are crucial in maintaining the glycemic balance. Alcohol could cause pancreatic β-cell apoptosis78 and dysfunction, decreasing insulin secretion, resulting in decreased circulating insulin levels.79,80 With the increase of alcohol amount, the damage of β-cells is gradually aggravated. Heavy alcohol intake could reduce the insulin-secretory ability of pancreatic islets,12 decrease glucokinase expression, and inhibit insulin receptor expression,11 promoting the development of T2DM. On the contrary, LMAC seems to be related with lower fasting insulin levels, a similar effect to that observed in healthy people, who are often considered to be associated with higher insulin sensitivity,81 showing as reduced fasting insulin concentrations by 19.2% and increased insulin sensitivity by 7.2% compared with non-drinkers.82 The reasons for low insulin levels related with MAC may be different in men and women, demonstrating as higher clearance of insulin in men and lower secretion of basal insulin in women.83 Presumably, heavy drinking may impair pancreatic β-cell function and disrupt insulin signaling pathways, contributing to the development of diabetes, while lower insulin levels in non-heavy drinkers seem helpful to maintain glycemic homeostasis. Binge drinking has been proven to be an independent risk factor for IR in MAFLD.84 In terms of mechanism, binge drinking impairs hypothalamic insulin signaling and decreases insulin secretion, playing a central role in increasing the risk of IR and T2DM. In addition, peripheral insulin dysfunction might be involved in IR. More studies are needed to further verify these hypotheses.

Though some studies showed a positive relation between alcohol consumption and the risk of IR and T2DM,8587 most studies suggest reduced risks of T2DM in individuals with LMAC. According to a recent umbrella review, high-quality evidence shows that MAC (12–24 g/day) is negatively correlated with the incidence of diabetes.88 Prospective and cross-sectional studies show a lower presence of IR and impaired glucose tolerance in obese individuals with MAC than in obese non-drinkers.20,89 Another cross-sectional study showed that LMAC did not decrease the risk of T2DM in obese individuals,90 indicating that the role of MAC in the regulation of glucose and lipid metabolism in obese people is controversial. Compared with women, men are more likely to benefit from LMAC.91,92 Men with cardiovascular disease risk factors can benefit from long-term red wine consumption (40 g/day) in several aspects, including decreased plasma insulin levels, improved glucose homeostasis, and increased HDL-cholesterol levels.69 Hence, LMAC seems to improve IR in individuals with a high risk of T2DM, especially in men. Interestingly, a reduced risk of T2DM in LMAC is often observed among regular drinkers. A study in Japan showed ∼4 drinks per drinking day for 4–7 days weekly in men resulted in a lower risk of T2DM compared with non-drinkers.93 In a large cohort study from Denmark, the lowest risk of T2DM was observed at 14 drinks/week in men and at 9 drinks/week in women. Compared with current alcohol consumers consuming <1 day per week, the consumption of alcohol for 3–4 days per week was associated with a significantly lower risk for diabetes in men.94

Alcohol may commonly impair pancreatic β-cell function. However, the risks of IR and T2DM are low in LMAC populations, as shown in several clinical studies, which is probably in part related with lifestyle. In a prospective cohort study with a 10-year follow-up in the Netherlands, individuals with LMAC (5.0–29.9 g/day for men and 5.0–14.9 g/day for women) exhibited a significantly lower risk of T2DM on the basis of one low-risk lifestyle behavior, and an approximately 40% reduced risk of T2DM on the basis of multiple low-risk lifestyle behaviors compared with non-drinkers.95 Another randomized clinical trial showed that MAC with lifestyle modification reduced the incidence rate of diabetes in individuals at high risk of diabetes (including impaired glucose tolerance, elevated fasting glucose, or BMI ≥24 kg/m2) after a 3-year follow-up.80 As is well known, metabolic dysfunction is often related to unhealthy lifestyles, e.g., high-fat diet, lack of exercise, and smoking. In the above studies, a healthy lifestyle often includes an ideal body weight, a healthy diet, moderate exercise, no smoking, and reduced total energy intake, which are helpful in restoring normal metabolism. Additionally, MAC is considered as a healthy behavior. Thus, benefits from LMAC further improve metabolism on the basis of these healthy lifestyles.

The beneficial effects of MAC on insulin sensitivity are not fully understood. The expression of some molecules may change during MAC and further influence glucose and lipid metabolism. Adiponectin, an insulin-sensitizing adipokine, has been confirmed to play important roles in maintaining insulin sensitivity and suppressing fatty acid synthesis.96 Hypoadiponectinemia is closely associated with IR in obesity and diabetes.97,98 Diet-intervention studies in small groups of young and middle-aged men with or without IR have shown increased adiponectin concentrations after MAC intervention.99,100 A large population study confirmed that adiponectin levels were higher in men with frequent MAC.100 Alcohol-induced increases in adiponectin improve insulin sensitivity and glucose metabolism and decrease the risk of IR. Therefore, an improved IR and a decreased risk of T2DM in MAC may be the result of multiple factors, including proper drinking frequencies, low-risk lifestyle, and the expression of molecules improving glucose metabolism.

Alcohol and blood pressure

Early studies have confirmed that chronic alcohol consumption affects blood pressure,101 manifesting as increased blood pressure in drinkers.102105 The increased risk of elevated blood pressure is associated with the amount of alcohol consumed. However, the “threshold” amount is not quite clear. According to recent studies, the potential “threshold” could not be high, as individuals with alcohol consumption more than 100 g/week show elevated systolic blood pressure (SBP).66 Chronic LMAC has a greater effect on awake blood pressure, increasing SBP and diastolic blood pressure (DBP) by about 2.5–3.0 mmHg and 2.0 mmHg, respectively, and a weaker effect on blood pressure during sleep, decreasing DBP by 2.0 mmHg.106,107 Though a study showed a higher risk of hypertension in MAC individuals than in light drinkers,67 the effect of chronic LMAC on hypertension, which has been investigated in human and animal models, is not that obvious.66,108,109 A population-based prospective study even showed a significantly lower incidence of hypertension in participants with LMAC after a 20-year follow-up compared with non-drinkers.110 Age is a well-known risk factor for blood pressure. Elderly people are often at higher risks of hypertension than young people. There is a similar effect of age on drinkers’ blood pressure.111 In young drinkers, elevated HDL-cholesterol levels (≥47 mg/dL) could be a protective factor for MAC, preventing significant increases in blood pressure.102 In two studies, the incidence of hypertension was higher in individuals who consumed large amounts of alcohol (20–30 g/day or more).102,103 In middle-aged men, an increased risk of hypertension, even in light drinkers (12 g/day), was observed, irrespective of the levels of HDL-cholesterol.103 With the increase of age, alcohol consumption ≥140 g/week is associated with significantly increased SBP (5–12 mmHg) and DBP (3–6 mmHg) and an increased risk of hypertension (OR: 1.83, 95% CI: 1.40–2.40) in older men.108 Therefore, age showed a similar negative relation with blood pressure in drinkers as in other populations. With increasing age, the protective effects of HDL-cholesterol and LMAC on blood pressure are gradually overshadowed by the increased risk of hypertension.

Both chronic heavy drinking and binge drinking (occasional or frequent) are related with an increased risk of hypertension in a dose-dependent manner, especially in men.52,67,112 Blood pressure is temporarily reduced after binge drinking within approximately 2–3 h, but it could dramatically increase after 24 h.113,114 An Asian cohort study showed that daily alcohol consumption exceeding 60 g/day significantly increased the risk of hypertension in men.102 However, a recent population-based study on conventional epidemiology and genetic epidemiology showed that lower amounts of alcohol intake were related with increased blood pressure; SBP was increased by 4.8 mmHg (to a level of about 135 mmHg, 95% CI: 4.5–5.1) and DBP by 4.3 mmHg (95% CI: 3.7–4.9) in men with 280 g/week alcohol intake. In women with similar alcohol intake, SBP and DBP increased by 6.7 mmHg (95% CI: 4.3–9.0) and 3.8 mmHg (95% CI: 2.5–5.1), respectively.66 Obviously, excessive alcohol intake is related with increased blood pressure, especially in male drinkers. Fortunately, the effects of alcohol consumption are reversible. A reduction in alcohol consumption could help to reduce blood pressure, especially in heavy drinkers. Individuals who drink six or more drinks per day could obtain a reduction in SBP by 5.5 mmHg and in DBP by approximately 4 mmHg if they reduce alcohol consumption by about 50%. Reductions in SBP and DBP are also achievable in other drinkers by reducing alcohol consumption, but to a lower degree.115 Though effects on blood pressure have been observed for both LMAC and heavy drinking, heavy drinking results in much stronger increases, often reaching blood pressures above 140/90 mmHg, with a significantly higher risk of hypertension compared with other drinkers.

Evidence of the effects of alcohol consumption on blood pressure is not as strong in women as in men. According to a recent systematic review and meta-analysis, female drinkers only account for 14% in clinical trials,115 indicating significant differences in gender distribution. Studies have indicated different effects of alcohol intake on blood pressure in female drinkers compared with male drinkers. Multivariate Cox proportional hazards analysis showed alcohol consumption was not necessarily associated with the risk of hypertension in women.104 Though MAC could elevate SBP and DBP in premenopausal women, the increase in SBP was not more than 2 mmHg and that in DBP was not more than 1.4 mmHg.116 Roerecke’s systematic review and meta-analysis have shown different incidences of hypertension in men and in women who drank 1–2 drinks/day (relative riskwomen vs. men=0.79; 95% CI: 0.67–0.93),117 indicating that women with LMAC were less likely to suffer from hypertension. The increased risk of hypertension was more obvious in women who exceeded two drinks per day.117 In older women, alcohol amounts below 140 g/week resulted in reductions in SBP of 3–5 mmHg and a reduced risk of hypertension (OR: 0.62, 95% CI: 0.53–0.72) compared with non-drinkers.108 These results suggest that chronic, regular LMAC in women tends to exert protective effects on blood pressure compared with men. However, data on alcohol consumption in female drinkers are not sufficient, especially in heavy drinkers. More research is needed to explore the relationship between alcohol intake and blood pressure in women.

The main mechanisms underlying the effects of alcohol on blood pressure include a direct effect of alcohol, alcohol metabolic-associated enzymes, and alcohol sensitivity. ADH1B and ALDH2 are two important enzymes in alcohol metabolism. Genetic polymorphisms of ADH1B (rs1229984) and ALDH2 (rs671) are related with the elimination rate of alcohol, alcohol sensitivity, and drinking behavior. The ADH1B*2 allele carrier, with enhanced enzyme activity, is related with more rapid alcohol elimination118,119 and, possibly, a reduced risk of hypertension and cardiovascular diseases.119,120 ALDH2 polymorphisms are considered to be associated with alcohol sensitivity and drinking behavior. Enzyme activity is weakened or lost in ALDH2*1/*2 (G/A) and ALDH2*2/*2 (A/A) allele carriers, slowing the process of alcohol metabolism, with higher alcohol sensitivity compared with the wild-type ALDH2*1 (G/G) carriers. In women, LMAC without alcohol sensitivity further decreases SBP by 2 mmHg and is associated with a lower risk of hypertension (OR: 0.62, 95% CI: 0.53–0.72) compared with LMAC with alcohol sensitivity (OR: 0.71, 95% CI: 0.60–0.83). Similarly, in men with alcohol consumption of 140 g/week or more, SBP and DBP were much higher in those with alcohol sensitivity (145 mmHg and 82 mmHg, respectively) than in those without alcohol sensitivity (138 mmHg and 79 mmHg, respectively) and non-drinkers (133 mmHg and 76 mmHg, respectively).108 The increased risk of hypertension in individuals with ALDH2 polymorphisms may be related with the rate of alcohol metabolism in part because slow elimination of alcohol enhances the effect of alcohol on blood pressure and partly reduces the blood pressure benefits of LMAC.

Limitations and expectations

Many studies show the beneficial effects of LMAC on metabolic functions. However, a recent combined analysis showed a linear relationship between alcohol consumption and all-cause mortality, with an increase in all-cause mortality among those who consumed more than 100 g/week.121 This dose is much lower than most guidelines’ recommendations and also lower than what is considered a “moderate” amount in most studies. Therefore, drinking in patients should be cautiously guided, especially in those with metabolic dysfunctions. For obese patients with MAFLD and decompensated liver cirrhosis, any amount of alcohol consumption is related with an increased risk of hepatocellular carcinoma.122,123 Alcohol drinking should be absolutely avoided in these patients.

Alcohol consumption is common in the MAFLD population and is related with metabolic dysfunction (Table 2). Interactions between alcohol and metabolic factors are complicated, and the benefits from non-heavy drinking may be reduced by other factors. A U-shaped or J-shaped relationship between alcohol consumption and the single component of metabolic dysfunction is common in many studies. In fact, there are probably more net-shaped relations among these factors than linear relations in real-world patients. As is well known, liver cirrhosis is an important stage during the development of chronic liver disease, and it is usually irreversible. Unfortunately, most studies on alcohol and MAFLD are focused on early-stage liver disease, and only a few studies focus on MAFLD with liver fibrosis or cirrhosis. Thus, the exact impacts of alcohol consumption (especially non-heavy drinking) on MAFLD and metabolic-associated impairments of target organs, complications, and even tumors are not quite clear. More research studies are needed to explore the long-term effects of alcohol consumption on end-stage MAFLD and metabolic syndrome, to fully understand the effects of alcohol consumption and guide patients who consume alcohol.

Table 2

Main clinical studies on alcohol and metabolic dysfunctions included in this review

Author and yearREFStudy typeFollow-upAlcohol beverageAmountPopulationMain indicatorsRalation typeMain results
Alcohol, obesity, and liver injury1Schütze M, 20099Prospective study8.5 yearsBeer1,000 mL/day7,876 men, 12,749 womenWCU-shapedMen consuming 1,000 mL/day beer were at 17% higher risk for WC gain compared with very light consumers.
2Inan-Eroglu E, 202019Cross-sectional studyRed wine; champagne and white wine; beer and cider; spirits; fortified wine<14 units/week for women and <21 units/week for menUK Biobank baseline data, n = 280,183, 48.3% femaleBMIThose drinking within the public health guidelines had a lower BMI by 1.34 kg/m2 (95% CI 1.42–1.26 kg/m2) compared to never drinkers.
3Wang L, 201021Prospective cohort study12.9 yearsNot mentioned0 ∼ ≥30 g/d19,220 US women aged 39 years and above with baseline BMI of 18.5–25 kg/m21. Overweight or obese (BMI ≥25 kg/m2). 2. Obese (BMI ≥30 kg/m2)Almost linearly inverse relationLMAC was associated with smaller weight gain and lower risk of becoming overweight and/or obese.
4Golan R, 201722Randomized controlled study2 yearsWine150 mL/dayn = 48, alcohol-abstaining adults with well-controlled T2DMBodyweight and abdominal adiposityModerate wine consumption did not promote weight gain or abdominal adiposity.
5Naveau S, 199729Retrospective study≥50 g/dayn = 1,604, patients with ALD. Biopsy-proven liver cirrhosis in most cases.Liver histologySynergistic effectThe presence of excess weight for at least 10 years was a risk factor for cirrhosis, acute alcoholic hepatitis, and steatosis.
6Kwon HK, 201434Cross-sectional study≤40 g/weekn = 77, obese patients with liver biopsy-proven NAFLDLiver histology, especially liver cirrhosisNegative relationAlcohol consumption of ≥24 gram-years was associated with less severe disease (fibrosis stage 3–4).
7Blomdahl J, 202140Cross-sectional study<140 g/weekn = 86, obese patients with biopsy-proven NAFLDAdvanced liver cirrhosisMAC was associated with advanced fibrosis. Patients with T2DM had the highest risk.
Alohol and lipid metabolism8Hiramine Y, 201148Cross-sectional studyNot mentioned0 ∼ ≥60 g/dayn = 9,886, men aged 30–69 yearsSerum TGU-shapedSerum TG was lower in former drinkers than non-drinkers and other drinkers. Serum TG was highest in heavy drinkers than other drinkers.
9Sierksma A, 200272Randomized, controlled, cross-over studyBeer40 g/day for men, 30 g/day for women10 middle-aged men and 9 postmenopausal womenApo A-I, HDL-cholesterol, and paraoxonase activitySerum apo A-I, HDL-cholesterol, and paraoxonase activity were significantly increased during 3 weeks of MAC compared with no alcohol consumption.
Alcohol and diabetes10Crandall JP, 200980Randomized controlled study3.2 yearsBeer, wine, and hard liquor<36 g/day, without heavy or binge drinkingn = 3,175, individuals at high risk of diabetesInsulin secretion and risk of diabetesInverse associationDaily MAC was associated with lower insulin secretion and reduced risk of incident diabetes.
11Davies MJ, 200282Randomized, controlled, cross-over study8 weeksEverclear in orange juice0, 15, or 30 g/dayn = 51, healthy postmenopausal womenInsulin level and sensitivity, TGInverse associationConsumption of 30 g/day of alcohol reduced fasting insulin by 19.2% and TG by 10.3%, and increased insulin sensitivity by 7.2% compared with 0 g/day.
12Joosten MM, 201095Prospective study10.3 yearsBeer, wine, and spirits0 ∼ ≥30 g/dayn = 35,625, Dutch adults at low risk of diabetesRisk of diabetesInverse associationOn the basis of multiple low-risk lifestyle behaviors, LMAC (5.0–14.9 g/day for women; 5.0–29.9 g/day for men) was associated with ≈40% lower risk compared with abstinence.
Alcohol and hypertension13Rodrigues P, 2018110Prospective studyOver 20 yearsBeer, wine, and spirits0 ∼ ≥14 drinks/week (1 drink = 14 g of pure ethanol)n = 2,368, individuals between 18 and 30 years of ageIncidence of hypertensionIncidence of hypertension was much lower in LMAC (<14 drink/wk) individuals.
14Mori TA, 2015116Randomized controlled, cross-over study4 weeks for each periodRed wine146 or 218 g/weekn = 24, women aged 25 to 49 years24-hour ambulatory blood pressurePositive relationHigh volume alcohol consumption was related with increased SBP (1.6–2 mmHg) and DBP (1.2–1.4 mmHg).
15Millwood IY, 201966Prospective studyAbout 10 yearsBeer, wine, and spirits0 ∼ >420 g/weekn = 512,715 Chinese adultsRisk of hypertensionIn individuals with per 280 g/week alcohol intake, SBP and DBP increased by 4.8 mmHg and 4.3 mmHg in men and by 6.7 mmHg and 3.8 mmHg in women, respectively.

Special attention should be paid to several populations. First is ex-drinkers and abstainers. The benefits from LMAC are often shown in current drinkers, usually accounting for the majority of participants in most studies. On the contrary, data on ex-drinkers and abstainers are not enough to analyze the impact of stopping alcohol consumption on metabolic factors well. Studies have shown changes of several metabolic factors after a period of abstinence, e.g., decreased HDL levels and visceral fat area and improved homeostasis, among moderate to heavy drinkers.124,125 Thus, it is necessary to evaluate the effects of abstinence on metabolism and re-evaluate the effects of LMAC on metabolism after abstinence. Second is female drinkers. There are more male drinkers than female drinkers in the real world and in most clinical trials. Usually, the non-drinkers are mainly female, while the drinkers are mainly male in most studies. With increasing amounts of alcohol consumption, the proportion of males increases dramatically, and the heavy drinkers are almost all men, especially in large, population-based studies.66,126,127 Thus, there is an almost inevitable sex bias because of the smaller female samples. As shown by some studies, the effects of alcohol are significantly different between male and female drinkers. There seems to be a much closer relationship between alcohol and male sex, including genetic epidemiological characteristics.128 Therefore, more studies are needed to evaluate the role of alcohol consumption on metabolism in female drinkers. Third is patients with borderline high blood pressure. A criterion of SBP ≥140 mmHg and/or DBP ≥90 mmHg or special drug treatment is considered for the diagnosis of hypertension in many studies. According to the new definition of MAFLD, a blood pressure of ≥135/85 mmHg is considered a metabolic risk abnormality,1 a more rigorous standard than the former. Therefore, the decreased risk of hypertension upon LMAC could possibly be overestimated in some individuals with other metabolic risk abnormalities. Individuals with blood pressure between 135/85 mmHg and 140/90 mmHg have shown an increased risk of metabolic dysfunctions.

In conclusion, alcohol drinking is closely related with metabolic dysfunction in several systems, such as the liver-gut axis, the liver-brain axis, the liver-pancreas axis, and the liver-adipose tissue axis (Fig. 1). LMAC combined with a healthy lifestyle may be helpful for maintaining metabolic homeostasis, while heavy drinking and binge drinking are two common dangerous drinking patterns that should be avoided. The new definition of MAFLD is a positive diagnosis of the disease with simple criteria. Though “alcohol” is excluded from the diagnosis, the relationship between MAFLD and alcohol is still close. Much attention should be paid to alcohol consumption during the management of MAFLD.

Relationship between alcohol consumption and metabolic dysfunctions.
Fig. 1  Relationship between alcohol consumption and metabolic dysfunctions.

Obesity: heavy drinking and binge drinking are associated with increased body weight and WC due to the obviously increased total energy intake and impaired peripheral or central insulin signaling pathways. LMAC is likely to maintain normal body weight mainly through improved IR. Liver injury: heavy or binge drinking in obese individuals exerts synergistic effects on liver injury. Liver-adipose tissue axis and liver-gut axis are two important mechanisms. The long-term effects of LMAC on liver cirrhosis are not quite clear. Lipid metabolism: alcohol is related with increased TG and HDL levels. However, the antioxidant effects of HDL are different, showing as enhanced antioxidative properties in LMAC and impaired antioxidative properties in heavy or binge drinkers with poor liver function. T2DM: heavy drinking and binge drinking are associated with increased risks of T2DM, mainly through impaired insulin signaling, decreased insulin secretory, and IR. Appropriate frequencies of LMAC, especially in combination with a healthy lifestyle, are related with improved IR and a decreased risk of T2DM, partly through regulating the expression of adiponectin. Hypertension: the effects of alcohol consumption on blood pressure are common. Heavy drinking and binge drinking are usually associated with significantly increased blood pressure and the risk of hypertension, while the risk of hypertension is lower in LMAC. ALD, alcoholic-related liver disease; CYP, Cytochrome P450; HDL, high-density lipoprotein; IR, insulin resistance; LMAC, light to moderate alcohol consumption; MAFLD, metabolic-associated fatty liver disease; T2DM, type 2 diabetes mellitus; TG, triglyceride; WC, waist circumference.



alcohol dehydrogenase


alcoholic-related liver disease


aldehyde dehydrogenase


5′-AMP-activated protein kinase


body mass index


confidence interval


cytochrome P450


diastolic blood pressure


high-density lipoprotein


hazard ratio




insulin resistance


light to moderate alcohol consumption


moderate alcohol consumption


metabolic-associated fatty liver disease


mechanistic target of rapamycin


mTOR complex 1


odds ratio


systolic blood pressure


sterol regulatory element-binding proteins


type 2 diabetes mellitus




tumor necrosis factor-α


waist circumference



None to declare.

Conflict of interest

The authors have no conflict of interest related to this publication.

Authors’ contributions

Writing the manuscript (FRS), and developing the idea for the article and critically revising it (BYW). All authors have read and approved the final version of the manuscript.


  1. Eslam M, Newsome PN, Sarin SK, Anstee QM, Targher G, Romero-Gomez M, et al. A new definition for metabolic dysfunction-associated fatty liver disease: an international expert consensus statement. J Hepatol 2020;73(1):202-209 View Article
  2. Eslam M, Sarin SK, Wong VW, Fan JG, Kawaguchi T, Ahn SH, et al. The Asian Pacific Association for the Study of the Liver clinical practice guidelines for the diagnosis and management of metabolic associated fatty liver disease. Hepatol Int 2020;14(6):889-919 View Article
  3. Chalasani N, Younossi Z, Lavine JE, Charlton M, Cusi K, Rinella M, et al. The diagnosis and management of nonalcoholic fatty liver disease: practice guidance from the American Association for the Study of Liver Diseases. Hepatology 2018;67(1):328-357 View Article
  4. European Association for the Study of the Liver, European Association for the Study of the Liver. EASL clinical practice guidelines: management of alcohol-related liver disease. J Hepatol 2018;69(1):154-181 View Article
  5. Singal AK, Bataller R, Ahn J, Kamath PS, Shah VH. ACG clinical guideline: alcoholic liver disease. Am J Gastroenterol 2018;113(2):175-194 View Article
  6. Grucza RA, Sher KJ, Kerr WC, Krauss MJ, Lui CK, McDowell YE, et al. Trends in adult alcohol use and binge drinking in the early 21st-century United States: a meta-analysis of 6 national survey series. Alcohol Clin Exp Res 2018;42(10):1939-1950 View Article
  7. Butler L, Popkin BM, Poti JM. Associations of alcoholic beverage consumption with dietary intake, waist circumference, and body mass index in US adults: national health and nutrition examination survey 2003-2012. J Acad Nutr Diet 2018;118(3):409-420.e3 View Article
  8. Coulson CE, Williams LJ, Brennan SL, Berk M, Kotowicz MA, Lubman DI, et al. Alcohol consumption and body composition in a population-based sample of elderly Australian men. Aging Clin Exp Res 2013;25(2):183-192 View Article
  9. Schütze M, Schulz M, Steffen A, Bergmann MM, Kroke A, Lissner L, et al. Beer consumption and the ‘beer belly’: scientific basis or common belief?. Eur J Clin Nutr 2009;63(9):1143-1149 View Article
  10. Alcácera MA, Marques-Lopes I, Fajó-Pascual M, Puzo J, Blas Pérez J, Bes-Rastrollo M, et al. Lifestyle factors associated with BMI in a Spanish graduate population: the SUN study. Obes Facts 2008;1(2):80-87 View Article
  11. Jang HB, Go MJ, Park SI, Lee HJ, Cho SB. Chronic heavy alcohol consumption influences the association between genetic variants of GCK or INSR and the development of diabetes in men: A 12-year follow-up study. Sci Rep 2019;9(1):20029 View Article
  12. Yang BC, Wu SY, Leung PS. Alcohol ingestion induces pancreatic islet dysfunction and apoptosis via mediation of FGF21 resistance. Ann Transl Med 2020;8(6):310 View Article
  13. Souza E Souza LP, Miranda AEDS, Hermsdorff HHM, Silva CSOE, Barbosa DA, Bressan J, et al. Binge drinking and overweight in brazilian adults - CUME project. Rev Bras Enferm 2020;73(Suppl 1):e20190316 View Article
  14. Park KY, Park HK, Hwang HS. Relationship between abdominal obesity and alcohol drinking pattern in normal-weight, middle-aged adults: the Korea National Health and Nutrition Examination Survey 2008-2013. Public Health Nutr 2017;20(12):2192-2200 View Article
  15. Lindtner C, Scherer T, Zielinski E, Filatova N, Fasshauer M, Tonks NK, et al. Binge drinking induces whole-body insulin resistance by impairing hypothalamic insulin action. Sci Transl Med 2013;5(170):170ra14 View Article
  16. Escrivá-Martínez T, Galiana L, Herrero R, Rodríguez-Arias M, Baños RM. Understanding the influence of eating patterns on binge drinking: a mediation model. Int J Environ Res Public Health 2020;17(24):9451 View Article
  17. Hara T, Seko Y, Iwai N, Inada Y, Tsuji T, Okuda T, et al. Comparison of the effect of light alcohol consumption on Japanese men with and without fatty liver. Biomed Rep 2019;11(5):191-198 View Article
  18. Sogabe M, Okahisa T, Nakagawa T, Fukuno H, Nakasono M, Tomonari T, et al. Influence of light alcohol consumption on lifestyle-related diseases: a predictor of fatty liver with liver enzyme elevation in Japanese females with metabolic syndrome. BMC Gastroenterol 2016;16:17 View Article
  19. Inan-Eroglu E, Powell L, Hamer M, O’Donovan G, Duncan MJ, Stamatakis E. Is there a link between different types of alcoholic drinks and obesity? an analysis of 280,183 UK biobank participants. Int J Environ Res Public Health 2020;17(14):5178 View Article
  20. VanWagner LB, Ning H, Allen NB, Ajmera V, Lewis CE, Carr JJ, et al. Alcohol use and cardiovascular disease risk in patients with nonalcoholic fatty liver disease. Gastroenterology 2017;153(5):1260-1272.e3 View Article
  21. Wang L, Lee IM, Manson JE, Buring JE, Sesso HD. Alcohol consumption, weight gain, and risk of becoming overweight in middle-aged and older women. Arch Intern Med 2010;170(5):453-461 View Article
  22. Golan R, Shelef I, Shemesh E, Henkin Y, Schwarzfuchs D, Gepner Y, et al. Effects of initiating moderate wine intake on abdominal adipose tissue in adults with type 2 diabetes: a 2-year randomized controlled trial. Public Health Nutr 2017;20(3):549-555 View Article
  23. Yeomans MR. Alcohol, appetite and energy balance: is alcohol intake a risk factor for obesity?. Physiol Behav 2010;100(1):82-89 View Article
  24. Schrieks IC, Stafleu A, Griffioen-Roose S, de Graaf C, Witkamp RF, Boerrigter-Rijneveld R, et al. Moderate alcohol consumption stimulates food intake and food reward of savoury foods. Appetite 2015;89:77-83 View Article
  25. Fromenty B, Vadrot N, Massart J, Turlin B, Barri-Ova N, Lettéron P, et al. Chronic ethanol consumption lessens the gain of body weight, liver triglycerides, and diabetes in obese ob/ob mice. J Pharmacol Exp Ther 2009;331(1):23-34 View Article
  26. Sayon-Orea C, Martinez-Gonzalez MA, Bes-Rastrollo M. Alcohol consumption and body weight: a systematic review. Nutr Rev 2011;69(8):419-431 View Article
  27. Lau K, Baumeister SE, Lieb W, Meffert PJ, Lerch MM, Mayerle J, et al. The combined effects of alcohol consumption and body mass index on hepatic steatosis in a general population sample of European men and women. Aliment Pharmacol Ther 2015;41(5):467-476 View Article
  28. Ekstedt M, Franzén LE, Holmqvist M, Bendtsen P, Mathiesen UL, Bodemar G, et al. Alcohol consumption is associated with progression of hepatic fibrosis in non-alcoholic fatty liver disease. Scand J Gastroenterol 2009;44(3):366-374 View Article
  29. Naveau S, Giraud V, Borotto E, Aubert A, Capron F, Chaput JC. Excess weight risk factor for alcoholic liver disease. Hepatology 1997;25(1):108-111 View Article
  30. Naveau S, Dobrin AS, Balian A, Njiké-Nakseu M, Nohra P, Asnacios A, et al. Body fat distribution and risk factors for fibrosis in patients with alcoholic liver disease. Alcohol Clin Exp Res 2013;37(2):332-338 View Article
  31. Parker R, Kim SJ, Im GY, Nahas J, Dhesi B, Vergis N, et al. Obesity in acute alcoholic hepatitis increases morbidity and mortality. EBioMedicine 2019;45:511-518 View Article
  32. Moriya A, Iwasaki Y, Ohguchi S, Kayashima E, Mitsumune T, Taniguchi H, et al. Roles of alcohol consumption in fatty liver: a longitudinal study. J Hepatol 2015;62(4):921-927 View Article
  33. Cao G, Yi T, Liu Q, Wang M, Tang S. Alcohol consumption and risk of fatty liver disease: a meta-analysis. PeerJ 2016;4:e2633 View Article
  34. Kwon HK, Greenson JK, Conjeevaram HS. Effect of lifetime alcohol consumption on the histological severity of non-alcoholic fatty liver disease. Liver Int 2014;34(1):129-135 View Article
  35. Mitchell T, Jeffrey GP, de Boer B, MacQuillan G, Garas G, Ching H, et al. Type and pattern of alcohol consumption is associated with liver fibrosis in patients with non-alcoholic fatty liver disease. Am J Gastroenterol 2018;113(10):1484-1493 View Article
  36. Yamada K, Mizukoshi E, Seike T, Horii R, Kitahara M, Sunagozaka H, et al. Light alcohol consumption has the potential to suppress hepatocellular injury and liver fibrosis in non-alcoholic fatty liver disease. PLoS One 2018;13(1):e0191026 View Article
  37. Dunn W, Sanyal AJ, Brunt EM, Unalp-Arida A, Donohue M, McCullough AJ, et al. Modest alcohol consumption is associated with decreased prevalence of steatohepatitis in patients with non-alcoholic fatty liver disease (NAFLD). J Hepatol 2012;57(2):384-391 View Article
  38. Sun F, Zhuang Z, Zhang D, Chen Y, Liu S, Gao N, et al. Chronic moderate alcohol consumption relieves high-fat high-cholesterol diet-induced liver fibrosis in a rat model. Clin Exp Pharmacol Physiol 2018;45(10):1046-1055 View Article
  39. Chang Y, Ryu S, Kim Y, Cho YK, Sung E, Kim HN, et al. Low levels of alcohol consumption, obesity, and development of fatty liver with and without evidence of advanced fibrosis. Hepatology 2020;71(3):861-873 View Article
  40. Blomdahl J, Nasr P, Ekstedt M, Kechagias S. Moderate alcohol consumption is associated with advanced fibrosis in non-alcoholic fatty liver disease and shows a synergistic effect with type 2 diabetes mellitus. Metabolism 2021;115:154439 View Article
  41. Corrêa LH, Heyn GS, Magalhaes KG. The impact of the adipose organ plasticity on inflammation and cancer progression. Cells 2019;8(7):662 View Article
  42. Abdelmegeed MA, Ha SK, Choi Y, Akbar M, Song BJ. Role of CYP2E1 in mitochondrial dysfunction and hepatic injury by alcohol and non-alcoholic substances. Curr Mol Pharmacol 2017;10(3):207-225 View Article
  43. Cho YE, Kim DK, Seo W, Gao B, Yoo SH, Song BJ. Fructose promotes leaky gut, endotoxemia, and liver fibrosis through ethanol-inducible cytochrome P450-2E1-mediated oxidative and nitrative stress. Hepatology 2021;73(6):2180-2195 View Article
  44. Yun JW, Son MJ, Abdelmegeed MA, Banerjee A, Morgan TR, Yoo SH, et al. Binge alcohol promotes hypoxic liver injury through a CYP2E1-HIF-1α-dependent apoptosis pathway in mice and humans. Free Radic Biol Med 2014;77:183-194 View Article
  45. Carmiel-Haggai M, Cederbaum AI, Nieto N. Binge ethanol exposure increases liver injury in obese rats. Gastroenterology 2003;125(6):1818-1833 View Article
  46. Zhou JY, Jiang ZA, Zhao CY, Zhen Z, Wang W, Nanji AA. Long-term binge and escalating ethanol exposure causes necroinflammation and fibrosis in rat liver. Alcohol Clin Exp Res 2013;37(2):213-222 View Article
  47. Chang Y, Cho YK, Kim Y, Sung E, Ahn J, Jung HS, et al. Nonheavy drinking and worsening of noninvasive fibrosis markers in nonalcoholic fatty liver disease: a cohort study. Hepatology 2019;69(1):64-75 View Article
  48. Hiramine Y, Imamura Y, Uto H, Koriyama C, Horiuchi M, Oketani M, et al. Alcohol drinking patterns and the risk of fatty liver in Japanese men. J Gastroenterol 2011;46(4):519-528 View Article
  49. Enomoto N, Ikejima K, Yamashina S, Enomoto A, Nishiura T, Nishimura T, et al. Kupffer cell-derived prostaglandin E(2) is involved in alcohol-induced fat accumulation in rat liver. Am J Physiol Gastrointest Liver Physiol 2000;279(1):G100-G106 View Article
  50. Nakajima T, Kamijo Y, Tanaka N, Sugiyama E, Tanaka E, Kiyosawa K, et al. Peroxisome proliferator-activated receptor alpha protects against alcohol-induced liver damage. Hepatology 2004;40(4):972-980 View Article
  51. Nath B, Levin I, Csak T, Petrasek J, Mueller C, Kodys K, et al. Hepatocyte-specific hypoxia-inducible factor-1α is a determinant of lipid accumulation and liver injury in alcohol-induced steatosis in mice. Hepatology 2011;53(5):1526-1537 View Article
  52. Lee K. Gender-specific relationships between alcohol drinking patterns and metabolic syndrome: the Korea national health and nutrition examination survey 2008. Public Health Nutr 2012;15(10):1917-1924 View Article
  53. Duly AM, Alani B, Huang EY, Yee C, Haber PS, McLennan SV, et al. Effect of multiple binge alcohol on diet-induced liver injury in a mouse model of obesity. Nutr Diabetes 2015;5(4):e154 View Article
  54. Liu G, Zhang Y, Liu C, Xu D, Zhang R, Cheng Y, et al. Luteolin alleviates alcoholic liver disease induced by chronic and binge ethanol feeding in mice. J Nutr 2014;144(7):1009-1015 View Article
  55. Caron A, Richard D, Laplante M. The roles of mTOR complexes in lipid metabolism. Annu Rev Nutr 2015;35:321-348 View Article
  56. Chen H, Shen F, Sherban A, Nocon A, Li Y, Wang H, et al. DEP domain-containing mTOR-interacting protein suppresses lipogenesis and ameliorates hepatic steatosis and acute-on-chronic liver injury in alcoholic liver disease. Hepatology 2018;68(2):496-514 View Article
  57. Li HH, Tyburski JB, Wang YW, Strawn S, Moon BH, Kallakury BV, et al. Modulation of fatty acid and bile acid metabolism by peroxisome proliferator-activated receptor α protects against alcoholic liver disease. Alcohol Clin Exp Res 2014;38(6):1520-1531 View Article
  58. You M, Arteel GE. Effect of ethanol on lipid metabolism. J Hepatol 2019;70(2):237-248 View Article
  59. Kirpich I, Ghare S, Zhang J, Gobejishvili L, Kharebava G, Barve SJ, et al. Binge alcohol-induced microvesicular liver steatosis and injury are associated with down-regulation of hepatic Hdac 1, 7, 9, 10, 11 and up-regulation of Hdac 3. Alcohol Clin Exp Res 2012;36(9):1578-1586 View Article
  60. Lee HI, Yun KW, Seo KI, Kim MJ, Lee MK. Scopoletin prevents alcohol-induced hepatic lipid accumulation by modulating the AMPK-SREBP pathway in diet-induced obese mice. Metabolism 2014;63(4):593-601 View Article
  61. Li X, Zhang Y, Jin Q, Xia KL, Jiang M, Cui BW, et al. Liver kinase B1/AMP-activated protein kinase-mediated regulation by gentiopicroside ameliorates P2X7 receptor-dependent alcoholic hepatosteatosis. Br J Pharmacol 2018;175(9):1451-1470 View Article
  62. Jiang Z, Zhou J, Zhou D, Zhu Z, Sun L, Nanji AA. The adiponectin-SIRT1-AMPK pathway in alcoholic fatty liver disease in the rat. Alcohol Clin Exp Res 2015;39(3):424-433 View Article
  63. Rasineni K, Thomes PG, Kubik JL, Harris EN, Kharbanda KK, Casey CA. Chronic alcohol exposure alters circulating insulin and ghrelin levels: role of ghrelin in hepatic steatosis. Am J Physiol Gastrointest Liver Physiol 2019;316(4):G453-G461 View Article
  64. Xiang AS, Kingwell BA. Rethinking good cholesterol: a clinicians’ guide to understanding HDL. Lancet Diabetes Endocrinol 2019;7(7):575-582 View Article
  65. Hong SW, Linton JA, Shim JY, Lee HR, Kang HT. Association of alcohol consumption pattern with risk of hypertension in Korean adults based on the 2010-2012 KNHANES. Alcohol 2016;54:17-22 View Article
  66. Millwood IY, Walters RG, Mei XW, Guo Y, Yang L, Bian Z, et al. Conventional and genetic evidence on alcohol and vascular disease aetiology: a prospective study of 500 000 men and women in China. Lancet 2019;393(10183):1831-1842 View Article
  67. Waśkiewicz A, Sygnowska E. Alcohol intake and cardiovascular risk factor profile in men participating in the WOBASZ study. Kardiol Pol 2013;71(4):359-365 View Article
  68. Kim SH, Abbasi F, Lamendola C, Reaven GM. Effect of moderate alcoholic beverage consumption on insulin sensitivity in insulin-resistant, nondiabetic individuals. Metabolism 2009;58(3):387-392 View Article
  69. Chiva-Blanch G, Urpi-Sarda M, Ros E, Valderas-Martinez P, Casas R, Arranz S, et al. Effects of red wine polyphenols and alcohol on glucose metabolism and the lipid profile: a randomized clinical trial. Clin Nutr 2013;32(2):200-206 View Article
  70. Gaziano JM, Buring JE, Breslow JL, Goldhaber SZ, Rosner B, VanDenburgh M, et al. Moderate alcohol intake, increased levels of high-density lipoprotein and its subfractions, and decreased risk of myocardial infarction. N Engl J Med 1993;329(25):1829-1834 View Article
  71. Sogabe M, Okahisa T, Taniguchi T, Tomonari T, Tanaka T, Tanaka H, et al. Light alcohol consumption plays a protective role against non-alcoholic fatty liver disease in Japanese men with metabolic syndrome. Liver Int 2015;35(6):1707-1714 View Article
  72. Sierksma A, van der Gaag MS, van Tol A, James RW, Hendriks HF. Kinetics of HDL cholesterol and paraoxonase activity in moderate alcohol consumers. Alcohol Clin Exp Res 2002;26(9):1430-1435 View Article
  73. Mäkelä SM, Jauhiainen M, Ala-Korpela M, Metso J, Lehto TM, Savolainen MJ, et al. HDL2 of heavy alcohol drinkers enhances cholesterol efflux from raw macrophages via phospholipid-rich HDL 2b particles. Alcohol Clin Exp Res 2008;32(6):991-1000 View Article
  74. Marmillot P, Munoz J, Patel S, Garige M, Rosse RB, Lakshman MR. Long-term ethanol consumption impairs reverse cholesterol transport function of high-density lipoproteins by depleting high-density lipoprotein sphingomyelin both in rats and in humans. Metabolism 2007;56(7):947-953 View Article
  75. Rao MN, Liu QH, Marmillot P, Seeff LB, Strader DB, Lakshman MR. High-density lipoproteins from human alcoholics exhibit impaired reverse cholesterol transport function. Metabolism 2000;49(11):1406-1410 View Article
  76. Phukan JP, Sinha A, Deka JP. Serum lipid profile in alcoholic cirrhosis: a study in a teaching hospital of north-eastern India. Niger Med J 2013;54(1):5-9 View Article
  77. Padro T, Muñoz-García N, Vilahur G, Chagas P, Deyà A, Antonijoan RM, et al. Moderate beer intake and cardiovascular health in overweight individuals. Nutrients 2018;10(9):1237 View Article
  78. Dembele K, Nguyen KH, Hernandez TA, Nyomba BL. Effects of ethanol on pancreatic beta-cell death: interaction with glucose and fatty acids. Cell Biol Toxicol 2009;25(2):141-152 View Article
  79. Kim JY, Song EH, Lee HJ, Oh YK, Park YS, Park JW, et al. Chronic ethanol consumption-induced pancreatic {beta}-cell dysfunction and apoptosis through glucokinase nitration and its down-regulation. J Biol Chem 2010;285(48):37251-37262 View Article
  80. Crandall JP, Polsky S, Howard AA, Perreault L, Bray GA, Barrett-Connor E, et al. Alcohol consumption and diabetes risk in the Diabetes Prevention Program. Am J Clin Nutr 2009;90(3):595-601 View Article
  81. Schrieks IC, Heil AL, Hendriks HF, Mukamal KJ, Beulens JW. The effect of alcohol consumption on insulin sensitivity and glycemic status: a systematic review and meta-analysis of intervention studies. Diabetes Care 2015;38(4):723-732 View Article
  82. Davies MJ, Baer DJ, Judd JT, Brown ED, Campbell WS, Taylor PR. Effects of moderate alcohol intake on fasting insulin and glucose concentrations and insulin sensitivity in postmenopausal women: a randomized controlled trial. JAMA 2002;287(19):2559-2562 View Article
  83. Bonnet F, Disse E, Laville M, Mari A, Hojlund K, Anderwald CH, et al. Moderate alcohol consumption is associated with improved insulin sensitivity, reduced basal insulin secretion rate and lower fasting glucagon concentration in healthy women. Diabetologia 2012;55(12):3228-3237 View Article
  84. Oh JE. Relationship between heavy drinking, binge drinking, and metabolic syndrome in obese and non-obese Korean male adults. Nutr Res Pract 2018;12(2):166-172 View Article
  85. Miyake T, Kumagi T, Hirooka M, Furukawa S, Yoshida O, Koizumi M, et al. Low alcohol consumption increases the risk of impaired glucose tolerance in patients with non-alcoholic fatty liver disease. J Gastroenterol 2016;51(11):1090-1100 View Article
  86. Yu H, Wang T, Zhang R, Yan J, Jiang F, Li S, et al. Alcohol consumption and its interaction with genetic variants are strongly associated with the risk of type 2 diabetes: a prospective cohort study. Nutr Metab (Lond) 2019;16:64 View Article
  87. Tatsumi Y, Morimoto A, Asayama K, Sonoda N, Miyamatsu N, Ohno Y, et al. Association between alcohol consumption and incidence of impaired insulin secretion and insulin resistance in Japanese: the Saku study. Diabetes Res Clin Pract 2018;135:11-17 View Article
  88. Neuenschwander M, Ballon A, Weber KS, Norat T, Aune D, Schwingshackl L, et al. Role of diet in type 2 diabetes incidence: umbrella review of meta-analyses of prospective observational studies. BMJ 2019;366:l2368 View Article
  89. Cotrim HP, Freitas LA, Alves E, Almeida A, May DS, Caldwell S. Effects of light-to-moderate alcohol consumption on steatosis and steatohepatitis in severely obese patients. Eur J Gastroenterol Hepatol 2009;21(9):969-972 View Article
  90. Metcalf PA, Scragg RK, Jackson R. Light to moderate alcohol consumption is protective for type 2 diabetes mellitus in normal weight and overweight individuals but not the obese. J Obes 2014;2014:634587 View Article
  91. Gunji T, Matsuhashi N, Sato H, Iijima K, Fujibayashi K, Okumura M, et al. Alcohol consumption is inversely correlated with insulin resistance, independent of metabolic syndrome factors and fatty liver diseases. J Clin Gastroenterol 2011;45(9):808-813 View Article
  92. Akahane T, Namisaki T, Kaji K, Moriya K, Kawaratani H, Takaya H, et al. Chronic alcohol consumption is inversely associated with insulin resistance and fatty liver in Japanese males. Nutrients 2020;12(4):1036 View Article
  93. Sato KK, Hayashi T, Harita N, Koh H, Maeda I, Endo G, et al. Relationship between drinking patterns and the risk of type 2 diabetes: the Kansai Healthcare Study. J Epidemiol Community Health 2012;66(6):507-511 View Article
  94. Holst C, Becker U, Jørgensen ME, Grønbæk M, Tolstrup JS. Alcohol drinking patterns and risk of diabetes: a cohort study of 70,551 men and women from the general Danish population. Diabetologia 2017;60(10):1941-1950 View Article
  95. Joosten MM, Grobbee DE, van der A DL, Verschuren WM, Hendriks HF, Beulens JW. Combined effect of alcohol consumption and lifestyle behaviors on risk of type 2 diabetes. Am J Clin Nutr 2010;91(6):1777-1783 View Article
  96. Awazawa M, Ueki K, Inabe K, Yamauchi T, Kaneko K, Okazaki Y, et al. Adiponectin suppresses hepatic SREBP1c expression in an AdipoR1/LKB1/AMPK dependent pathway. Biochem Biophys Res Commun 2009;382(1):51-56 View Article
  97. Bu J, Feng Q, Ran J, Li Q, Mei G, Zhang Y. Visceral fat mass is always, but adipokines (adiponectin and resistin) are diversely associated with insulin resistance in Chinese type 2 diabetic and normoglycemic subjects. Diabetes Res Clin Pract 2012;96(2):163-169 View Article
  98. Aleidi S, Issa A, Bustanji H, Khalil M, Bustanji Y. Adiponectin serum levels correlate with insulin resistance in type 2 diabetic patients. Saudi Pharm J 2015;23(3):250-256 View Article
  99. Beulens JW, de Zoete EC, Kok FJ, Schaafsma G, Hendriks HF. Effect of moderate alcohol consumption on adipokines and insulin sensitivity in lean and overweight men: a diet intervention study. Eur J Clin Nutr 2008;62(9):1098-1105 View Article
  100. Sierksma A, Patel H, Ouchi N, Kihara S, Funahashi T, Heine RJ, et al. Effect of moderate alcohol consumption on adiponectin, tumor necrosis factor-alpha, and insulin sensitivity. Diabetes Care 2004;27(1):184-189 View Article
  101. Puddey IB, Beilin LJ, Vandongen R, Rouse IL, Rogers P. Evidence for a direct effect of alcohol consumption on blood pressure in normotensive men. A randomized controlled trial. Hypertension 1985;7(5):707-713 View Article
  102. Dakeishi M, Murata K, Tamura A, Iwata T. Relation between benchmark dose and no-observed-adverse-effect level in clinical research: effects of daily alcohol intake on blood pressure in Japanese salesmen. Risk Anal 2006;26(1):115-123 View Article
  103. Nakanishi N, Makino K, Nishina K, Suzuki K, Tatara K. Relationship of light to moderate alcohol consumption and risk of hypertension in Japanese male office workers. Alcohol Clin Exp Res 2002;26(7):988-994 View Article
  104. Ohmori S, Kiyohara Y, Kato I, Kubo M, Tanizaki Y, Iwamoto H, et al. Alcohol intake and future incidence of hypertension in a general Japanese population: the Hisayama study. Alcohol Clin Exp Res 2002;26(7):1010-1016 View Article
  105. Wakabayashi I. Influence of body weight on the relationships of alcohol drinking with blood pressure and serum lipids in women. Prev Med 2009;49(5):374-379 View Article
  106. Zilkens RR, Burke V, Hodgson JM, Barden A, Beilin LJ, Puddey IB. Red wine and beer elevate blood pressure in normotensive men. Hypertension 2005;45(5):874-879 View Article
  107. Mori TA, Burke V, Zilkens RR, Hodgson JM, Beilin LJ, Puddey IB. The effects of alcohol on ambulatory blood pressure and other cardiovascular risk factors in type 2 diabetes: a randomized intervention. J Hypertens 2016;34(3):421-428;discussion 428 View Article
  108. Zhang WS, Jiang CQ, Cheng KK, Adab P, Thomas GN, Liu B, et al. Alcohol sensitivity, alcohol use and hypertension in an older Chinese population: the Guangzhou biobank cohort study. Hypertens Res 2009;32(9):741-747 View Article
  109. Cowpland C, Su GM, Murray M, Puddey IB, Croft KD. Effect of alcohol on cytochrome P450 arachidonic acid metabolism and blood pressure in rats and its modulation by red wine polyphenolics. Clin Exp Pharmacol Physiol 2006;33(3):183-188 View Article
  110. Rodrigues P, Santos-Ribeiro S, Teodoro T, Gomes FV, Leal I, Reis JP, et al. Association between alcohol intake and cardiac remodeling. J Am Coll Cardiol 2018;72(13):1452-1462 View Article
  111. Wakabayashi I, Araki Y. Influences of gender and age on relationships between alcohol drinking and atherosclerotic risk factors. Alcohol Clin Exp Res 2010;34(Suppl 1):S54-60 View Article
  112. Jung MH, Shin ES, Ihm SH, Jung JG, Lee HY, Kim CH. The effect of alcohol dose on the development of hypertension in Asian and Western men: systematic review and meta-analysis. Korean J Intern Med 2020;35(4):906-916 View Article
  113. Barden AE, Croft KD, Beilin LJ, Phillips M, Ledowski T, Puddey IB. Acute effects of red wine on cytochrome P450 eicosanoids and blood pressure in men. J Hypertens 2013;31(11):2195-2202;discussion 2202 View Article
  114. Wakabayashi I, Marumo M, Nonaka D, Shimomura T, Eguchi R, Lee LJ, et al. Potential biomarker peptides associated with acute alcohol-induced reduction of blood pressure. PLoS One 2016;11(1):e0147297 View Article
  115. Roerecke M, Kaczorowski J, Tobe SW, Gmel G, Hasan OSM, Rehm J. The effect of a reduction in alcohol consumption on blood pressure: a systematic review and meta-analysis. Lancet Public Health 2017;2(2):e108-e120 View Article
  116. Mori TA, Burke V, Beilin LJ, Puddey IB. Randomized controlled intervention of the effects of alcohol on blood pressure in premenopausal women. Hypertension 2015;66(3):517-523 View Article
  117. Roerecke M, Tobe SW, Kaczorowski J, Bacon SL, Vafaei A, Hasan OSM, et al. Sex-specific associations between alcohol consumption and incidence of hypertension: a systematic review and meta-analysis of cohort studies. J Am Heart Assoc 2018;7(13):e008202 View Article
  118. Yokoyama A, Yokoyama T, Matsui T, Mizukami T, Matsushita S, Higuchi S, et al. Alcohol dehydrogenase-1B genotype (rs1229984) is a strong determinant of the relationship between body weight and alcohol intake in Japanese alcoholic men. Alcohol Clin Exp Res 2013;37(7):1123-1132 View Article
  119. Gepner Y, Golan R, Harman-Boehm I, Henkin Y, Schwarzfuchs D, Shelef I, et al. Effects of initiating moderate alcohol intake on cardiometabolic risk in adults with type 2 diabetes: a 2-year randomized, controlled trial. Ann Intern Med 2015;163(8):569-579 View Article
  120. Holmes MV, Dale CE, Zuccolo L, Silverwood RJ, Guo Y, Ye Z, et al. Association between alcohol and cardiovascular disease: Mendelian randomisation analysis based on individual participant data. BMJ 2014;349:g4164 View Article
  121. Wood AM, Kaptoge S, Butterworth AS, Willeit P, Warnakula S, Bolton T, et al. Risk thresholds for alcohol consumption: combined analysis of individual-participant data for 599 912 current drinkers in 83 prospective studies. Lancet 2018;391(10129):1513-1523 View Article
  122. Ascha MS, Hanouneh IA, Lopez R, Tamimi TA, Feldstein AF, Zein NN. The incidence and risk factors of hepatocellular carcinoma in patients with nonalcoholic steatohepatitis. Hepatology 2010;51(6):1972-1978 View Article
  123. Kimura T, Tanaka N, Fujimori N, Sugiura A, Yamazaki T, Joshita S, et al. Mild drinking habit is a risk factor for hepatocarcinogenesis in non-alcoholic fatty liver disease with advanced fibrosis. World J Gastroenterol 2018;24(13):1440-1450 View Article
  124. Mehta G, Macdonald S, Cronberg A, Rosselli M, Khera-Butler T, Sumpter C, et al. Short-term abstinence from alcohol and changes in cardiovascular risk factors, liver function tests and cancer-related growth factors: a prospective observational study. BMJ Open 2018;8(5):e020673 View Article
  125. Funayama T, Tamura Y, Takeno K, Kawaguchi M, Kakehi S, Watanabe T, et al. Effects of alcohol abstinence on glucose metabolism in Japanese men with elevated fasting glucose: a pilot study. Sci Rep 2017;7:40277 View Article
  126. Chevli PA, Aladin AI, Kanaya AM, Kandula NR, Malaver D, Herrington DM. Alcohol consumption and subclinical atherosclerosis among South Asians: findings from the mediators of atherosclerosis in south Asians living in America (MASALA) study. Nutr Metab Cardiovasc Dis 2020;30(1):123-131 View Article
  127. Zhang X, Liu Y, Li S, Lichtenstein AH, Chen S, Na M, et al. Alcohol consumption and risk of cardiovascular disease, cancer and mortality: a prospective cohort study. Nutr J 2021;20(1):13 View Article
  128. Wang D, Zou Y, Yu S, Lin S, Li H, Yin Y, et al. The effect of ALDH2 rs671 gene mutation on clustering of cardiovascular risk factors in a big data study of Chinese population: associations differ between the sexes. BMC Cardiovasc Disord 2020;20(1):509 View Article
  • Journal of Clinical and Translational Hepatology
  • pISSN 2225-0719
  • eISSN 2310-8819

Alcohol and Metabolic-associated Fatty Liver Disease

Fu-Rong Sun, Bing-Yuan Wang
  • Reset Zoom
  • Download TIFF