Table 1.
Characteristics of studies evaluating anti-inflammatory, antioxidant, and antithrombotic effects of alcohol.
Reference | Design, Subjects (No), Follow-up | Population | Primary Outcome | Main Results |
---|---|---|---|---|
Anti-inflammatory and antioxidant effects | ||||
OBSERVATIONAL STUDIES | ||||
Nova et al. [33] | Observational, cross-sectional study, 143 participants. Participants were classified as abstainers and occasional consumers; predominantly beer consumers, and mixed beverage consumers (including wine, beer, and liquor). | Healthy adults 55 years of age and older. Spain. | Glucose, lipid profile, iron, transferrin, ferritin, and hs-CRP, VCAM-1, ICAM-1, P-selectin, E-selectin, IL-1β, IL-6, IL-8, IL-10, leptin, and adiponectin. | Consumption of alcohol: <25 g/d women and <40 g/d men. Mixed group: HDL-c and P-selectin compared with the abstainers’ group. Adiponectin compared with the beer group. |
Howard et al. [34] | Cross-sectional, 48,023 participants. NHANES laboratory and questionnaire data from the nine surveys between 1999 and 2016. | All participants aged 18 years or older. USA. | Demographic, socioeconomic, and lifestyle factors associated with the magnitude of NLR. | NLR: Non-drinkers (zero drinking d/y): 2.06 Frequent drinkers (>100 drinking d/y): 2.01 Less frequent drinkers (<100 drinking d/y): 1.95–1.96 |
Hamed et al. [36] | Prospective, nonrandomized, and observational study, 14 participants consumed 250 mL red wine daily for 21 consecutive days. | Healthy volunteers. Israel. | Vascular endothelial function, plasma SDF1a concentrations, circulating EPCs and FC. | Moderate intake of RW (1–2 glasses/d) increased EPC migration and proliferation, NO production and decreased extent of apoptosis. |
Barbaresko et al. [37] | Cohort study, 112 participants, mean follow-up of 1.7 years. | Northern German study population aged between 18 and 80 years. | CRP and IL-6 as response variables were used to derive dietary patterns. | Consumption of alcohol was associated with increase of CRP (OR 2.20; 95% CI 1.12, 4.35) and IL-6 (OR 3.14; 95% CI 1.26, 7.87). |
Da Luz et al. [38] | Cohort study, 354 participants, follow-up of 5.5 years. | All males (200 healthy RW drinkers and 154 abstainers) aged 50–70 years. Brazil. | The composite endpoint of total death, AMI, or MACE was assessed. | RW drinkers (28.9 ± 15g/d) showed higher HDL and LDL but lower CRP than abstainers. |
INTERVENTIONAL STUDIES | ||||
Chiva-Blanch et al. [39] | Randomized, crossover consumption trial, 67 volunteers. After a washout period, the subjects received 30 g alcohol/d of RW, DRW, or gin for 4 wk. | High-risk, male volunteers between 55 and 75 y old recruited at Hospital Clinic of Barcelona. | Seven cellular and 18 serum inflammatory biomarkers were evaluated. | Moderate consumption of RW (30 g alcohol/d): Phenolic compounds modulate leukocyte adhesion molecules. Ethanol and polyphenols of RW modulate ICAM-1, IL-6, E-selectin |
Estruch et al. [40] | Randomized cross-over trial. Forty participants received 30 g/ethanol/d as either wine or gin for 28 days. | Healthy men. Mean age, 38 years. Barcelona, Spain. | Serum vitamins, MDA, SOD, and glutathione peroxidase activities, lipid profile, oxidized LDL and LDL resistance to ex vivo oxidative stress. | RW (30 g/ethanol/d) intake: SOD activity (–8.1 U/gHb (95% confidence interval, CI, –138 to –25; p = 0.009)) and MDA levels (–11.9 nmol/L (CI, –21.4 to–2.5; p = 0.020)). |
Stote et al. [41] | Randomized crossover design, 53 volunteers consumed a weight-maintaining diet plus 0, 15, and 30 g/day of alcohol for 8 weeks. | Women older than 50 years of age; postmenopausal (last menses ≥12 months before the beginning of the study). | s-ICAM, hs-CPR, IL-6 fibrinogen, PAI-1, D-dimer, Factor VII c, CRP, IL-6 | After intake of 15 g and 30 g of alcohol, women showed decreased s-ICAM (5% and 5%), fibrinogen (4% and 6%), D-dimer (24% only for 30 g), and increased PAI-1 (27% and 54%). No difference for Factor VIIc, CRP, and IL-6. |
Roth et al. [42] | Randomized, controlled, crossover study, 38 volunteers were randomized to receive 30 g of ethanol/day as AWW or gin for 3 weeks. | High-risk male volunteers between 55 and 80 y old recruited at primary care centers associated with Hospital Clinic of Barcelona. | Classical cardiovascular risk factors, cellular expression of circulating adhesion molecules, EPCs, and plasma biomarkers. | AWW (30 g ethanol/day) shows a greater ability to repair and maintain endothelial integrity compared with gin (39.6% increase in EPCs). |
Anti-thrombotic effects | ||||
OBSERVATIONAL STUDIES | ||||
Lawlor et al. [43] | Causal associations in a cross-sectional study, 54,604 participants, Copenhagen General Population Study. | Danish General Population, mean age 56 years | BMI, BP, lipids, fibrinogen, and glucose | Non-drinkers were weakly associated with higher levels of fibrinogen. |
Wakabayashi, [44] | Cross-sectional, 6508 participants. | Men aged 30–69 years. Japan. | BMI, Platelet count, leukocyte count, GGT | Mean platelet counts in drinkers, at any level of intake, were not significantly different from that in non-drinkers |
Smith et al. [45] | Prospective, nonrandomized observational study, 54 volunteers. | Healthy volunteers, older than 21 years. | TEG-PM, maximal platelet activation, full platelet inhibition, ADP receptor agonist, or AA receptor agonist activation. | Acute alcohol consumption (maximum 2 g/kg) is associated with ADP receptor-mediated platelet inhibition in men, but not in women. |
INTERVENTIONAL STUDIES | ||||
Chiva-Blanch et al. [46] | Randomized, crossover consumption trial, 67 volunteers. After a washout period, the subjects received 30 g alcohol/d of RW, DRW, or gin for 4 weeks. | High-risk, male volunteers between 55 and 75 y old recruited at Hospital Clinic of Barcelona. | Fasting plasma glucose and insulin, HOMA-IR, plasma lipoproteins, apolipoproteins, and adipokines. | Beneficial effect of the polyphenols on insulin resistance (insulin and HOMA-IR for RW and DRW) with consumption of 30 g alcohol/d. |
ADP: adenosin diphosphate; AWW, aged white wine; AMI, acute myocardial infarction; Apo-AI, apolipoprotein; BMI, body mass index; CHD, coronary heart disease; CI: confidence interval; CPR, C-reactive protein; CV, cardiovascular; DRW, dealcoholized red wine; EPC, endothelial progenitor cell; FC, flow cytometry; GGT, gamma glutamyl transpeptidase; HDL-C, high-density lipoprotein cholesterol; HOMA-IR, homeostasis model assessment of insulin resistance; HTG, hypertriglyceridemia; ICAM-1, intercellular adhesion molecule 1; IL, interleukin; LDL-C, low-density lipoprotein cholesterol; MACE, major adverse cardiovascular events; MDA, malondialdehyde; NLR, neutrophil-to-lymphocyte ratio; PAI-1, Plasminogen activator inhibitor-1; RW, red wine; SOD, superoxide dismutase; TC, total cholesterol; TEG-PM, Thromboelastography with platelet mapping; TG, triglycerides; VCAM-1, vascular cell adhesion molecule 1. SDF1a, stromal cell-derived factor-1.