Elsevier

Atherosclerosis

Volume 208, Issue 2, February 2010, Pages 297-304
Atherosclerosis

Review
Wine and oxidative stress: Up-to-date evidence of the effects of moderate wine consumption on oxidative damage in humans

https://doi.org/10.1016/j.atherosclerosis.2009.06.031Get rights and content

Abstract

Wine and alcohol consumption has been considered to be protective against coronary heart disease development, an oxidative stress associated disease. Wine contains polyphenols displaying antioxidant properties tested in in vitro and in vivo studies. Due to this, a general consensus exists, both among the general public and the scientific community, that wine, particularly red wine, is an antioxidant beverage. Alcohol consumption, however, is associated with oxidative damage. Several studies have been carried out on the antioxidant health benefits of wine and wine polyphenols. However, adequate scientific evidence (Level I or II) is required to be provided before recommendations or statements which can reach the general public can be formulated. Here, we summarize the state of the art of the up-to-date body of knowledge, and the extent to which there exists evidence of the benefits of moderate wine consumption on oxidative damage in humans. From the available data, there is no evidence, at present, that sustained wine consumption provides antioxidant benefits in healthy volunteers other than to counteract a possible pro-oxidative effect of the alcohol. On the contrary, data on the antioxidant protective effect of red wine in oxidative stress situations are promising. In this way, the postprandial oxidative stress after a meal, despite the diversity of biomarkers used for its evaluation, is counteracted by the ingestion of wine. Further studies are warranted.

Introduction

Wine and alcohol consumption has been considered to be protective against coronary heart disease development, an oxidative stress associated disease [for review see [1]]. Wine is a complex matrix and may be considered as a phyto-complex to which ethanol has been added following natural fermentation [2]. Lifestyle habits in European Mediterranean countries have suffered changes in recent decades. However, wine remains the preferential pattern of alcohol consumption in these countries [3]. This pattern could also have a role, within the frame of the Mediterranean Diet, to explain the low incidence rates of coronary heart disease (CHD) in the Southern European countries in comparison with those observed in the Northern ones, Canada, or the USA [4]. In this way, Spanish regional diversity in wine consumption has been pointed out as one of the explanatory factors for the differences in myocardial infarction incidence rates observed among Spanish areas in ecological analyses [3].

Moderate amounts of alcohol markedly reduce the risk of CHD [for review see [1]]. The plausible mechanisms are first, the increase in high-density lipoprotein (HDL) cholesterol due to alcohol, and second, alcohol consumption also favourably affects the clotting and thrombolytic processes [1]. Data on the in vivo oxidative damage linked to moderate alcohol consumption are controversial. In a cross-sectional study, alcohol consumption was in a direct relationship with the plasma concentration of in vivo oxidized low-density lipoproteins (LDL) [5], but the levels of the DNA oxidation marker 8-oxo-deoxyguanosine have been reported to decrease with the amount of alcohol consumed [6]. In intervention studies a change in daily beer alcohol consumption from a moderate-heavy intake to a light one lowered the plasma F2-isoprostanes in healthy non-smoking men [7]. In other human intervention studies, consumption of beer or spirits at daily moderate doses of 30 g/day [8] or 40 g/day [9], but not at doses of 15 g/day [8], promoted only a marginal increase in urinary F2-isoprostanes. Ethanol metabolism can produce free radicals and reduce the levels of glutathione, the major cellular protection against oxidative stress [10]. In addition to alcohol wine contains polyphenols with antioxidant properties which could confer it with beneficial properties for health versus other types of alcohol consumption [1], [2]. Thus, the key questions are: (1) could polyphenols present in wine counteract an oxidative effect of alcohol?, and (2) could polyphenols present in wine provide additional benefits on oxidative stress and oxidative damage other than to counteract the possible oxidative effect of alcohol?

A large number of studies, both in experimental models and in humans, have been performed to ascertain the antioxidant properties of wine. A general consensus exists concerning the benefits of wine consumption, particularly red wine, on oxidative damage. However, the precepts of the Evidence-Based Medicine require high level scientific evidence to be provided before recommendations or statements for the general public can be formulated. The scientific evidence required is only provided by human, randomized, placebo-controlled, double-blind, clinical trials (Level I of Evidence) and, to some extent, by large cohort studies (Level II of Evidence) [11]. Of course, the level of evidence of a particular study depends not only on its type of design, but also on the quality of the study (external and internal validity, homogeneity of the sample, and statistical power). Finally, evidence is built by the agreement of the results of several similar studies [11]. Here, we summarize the state of the art of the body of knowledge and the extent to which we possess evidence of the antioxidant benefits of wine consumption in humans.

Section snippets

Wine components and oxidative damage

Mechanisms by which wine components, namely ethanol and polyphenols, could interact with reactive oxygen species (ROS) and oxidative damage are shown in Fig. 1. ROS oxidize lipids, proteins, and DNA. Oxidation of LDL lipoproteins is a hallmark for atherosclerosis and CHD development [12], and mutagenesis from DNA oxidative damage is considered to be a crucial step in human carcinogenesis [13]. Somatic DNA mutations, promoted by DNA oxidation, are considered to be involved in the atherosclerotic

Phenolic compounds in wine

The level of phenolic compounds in a wine is highly variable due to differences in variety and grape sources as well as processing. Red wine contains a higher concentration (around 10-fold) of polyphenols than white wine because during the wine making process, unlike white wine, red wine is macerated for weeks with the skin and seeds and these contain most of the phenolic compounds [24]. Concentrations of phenolic compounds in red wine range from around 1.2 to 3.0 g/L. The major phenolic

Bioavailability and disposition of phenolic compounds from wine in humans

It has been suggested that non-absorbable phenolic compounds may display local antioxidant activities in the gastrointestinal tract [26]. However, one of the prerequisites for assessing the physiological significance of phenolic compounds from wine is to determine their bioavailability and disposition in humans.

Phenolic compounds such as caffeic and gallic acids, quercetin, catechin, kaempherol, malvidin-3-glucoside, and resveratrol have been detected and quantified in human biological fluids

Human studies on the effect of wine consumption on oxidative stress

We searched MEDLINE for clinical studies assessing the effect either of acute (single dose) or sustained wine consumption on oxidative stress markers. Cohort studies aimed at assessing the relationship of wine consumption and oxidative stress markers were also looked for, but none was obtained. The following Medical Subject Heading Terms: wine, oxidative stress, oxidation, oxidative damage, LDL oxidation, lipid peroxidation, DNA oxidation, plasma antioxidant capacity, human, healthy, volunteers

Summary of findings

There are extensive differences in the methods and markers used among the studies reviewed. Few of them have been performed with sensitive biomarkers of in vivo oxidative damage or with markers which have been shown to be predictors for oxidative stress associated diseases. Despite a general consensus attributing antioxidant benefits in healthy volunteers to sustained wine consumption, there is no evidence, at present, that sustained wine consumption provides antioxidant benefits other than to

Acknowledgement

The CIBER de Fisiopatología de la Obesidad y Nutrición is an initiative of the Instituto de Salud Carlos III (ISCIII), Madrid, Spain.

References (70)

  • J.H.M. De Vries et al.

    Red wine is a poor source of bioavailable phenol in men

    J Nutr

    (2001)
  • J.L. Donovan et al.

    Catechin is present as metabolites in human plasma after consumption of red wine

    J Nutr

    (1999)
  • P. Pignatelli et al.

    Polyphenols synergistically inhibit oxidative stress in subjects given red and white wine

    Atherosclerosis

    (2006)
  • R. Zamora-Ros et al.

    Resveratrol metabolites in urine as a biomarker of wine intake in free-living subjects

    Free Radic Bio Med

    (2009)
  • A.J. Day et al.

    Conjugation position of quercetin glucuronides and effect on biological activity

    Free Radic Biol Med

    (2000)
  • R.A.A. Caccetta et al.

    Ingestion of red wine significantly increases plasma phenolic acid concentrations but does not acutely affect ex vivo lipoprotein oxidability

    Am J Clin Nutr

    (2000)
  • S. Maxwell et al.

    Red wine and antioxidant activity in serum

    Lancet

    (1994)
  • F. Natella et al.

    Red wine mitigates the postprandial increase of LDL susceptibility to oxidation

    Free Radic Biol Med

    (2001)
  • D.M. Blackhurst et al.

    Concomitant consumption of red wine and polyunsaturated fat acids in edible oils does not influence the peroxidation status of chylomicron lipids despite increasing plasma catechin concentration

    Nutr Met Cardiovasc Dis

    (2006)
  • G. Addolorato et al.

    Effects of short-term moderate alcohol administration on oxidative stress and nutritional status in healthy males

    Appetite

    (2008)
  • E. Guarda et al.

    Red wine reduces oxidative stress in patients with acute coronary syndrome

    Int J Cardiol

    (2005)
  • T. Weinbrenner et al.

    High oxidative stress in patients with stable coronary heart disease

    Atherosclerosis

    (2003)
  • B. Halliwell

    Are polyphenols antioxidants or pro-oxidants? What do we learn from cell culture and in vivo studies?

    Arch Biochem Biophys

    (2008)
  • K. Shimada et al.

    Circulating oxidized low-density lipoprotein is an independent predictor for cardiac event in patients with coronary heart disease

    Atherosclerosis

    (2004)
  • E. Sacanella et al.

    Down-regulation of adhesion molecules and other inflammatory biomarkers after moderate wine consumption in healthy women: a randomized trial

    Am J Clin Nutr

    (2007)
  • M. Vázquez-Agell et al.

    Inflammatory markers of atherosclerosis are decreased after moderate consumption of cava (sparkling wine) in men with low cardiovascular risk

    J Nutr

    (2007)
  • M.I. Covas

    The mediterranean diet and the role of alcohol

  • F. Rodríguez Artalejo et al.

    Lower consumption of wine and fish as a possible explanation for higher ischemic heart disease mortality in Spain's Mediterranean region

    Int J Epidemiol

    (1996)
  • R. Yoshida et al.

    Moderate alcohol consumption reduces urinary 8-hydroxydeoxyguanosine by inducing of uric acid

    Ind Health

    (2001)
  • T.J. Hartman et al.

    Moderate alcohol consumption and levels of antioxidant vitamins and isoprostanes in postmenopausal women

    Eur J Clin Nutr

    (2005)
  • L.A. Videla et al.

    Alcohol ingestion, liver glutathione and lipoperoxidation: metabolic interrelations and pathological implications

    Life Sci

    (1987)
  • J.L. Witzum

    The oxidation hypothesis of atherosclerosis

    Lancet

    (1994)
  • M.S. Cooke et al.

    Oxidative DNA damage: mechanisms, mutation, and disease

    FASEB J

    (2003)
  • M.A. Andreassi

    Coronary atherosclerosis and somatic mutations: an overview of the contributive factors for oxidative DNA damage

    Mutat Res

    (2003)
  • K. Nagata et al.

    Common pathogenic mechanisms in the development progression of liver injury caused by non-alcoholic or alcoholic steatohepatitis

    J Toxicol Sci

    (2007)
  • Cited by (0)

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