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Effects of alcohol-free beer on lipid profile and parameters of oxidative stress and inflammation in elderly women
Abstract
We assessed the influence of alcohol-free beer on factors implicated in atherosclerosis, such as lipid profile, oxidative stress parameters, and proinflammatory cytokines, in postmenopausal women, a population particularly at risk for atherosclerotic disease.
The study was carried out in 29 nuns, 58 to 73 y old, who live in a convent with a disciplined, regular, and homogeneous lifestyle. The nuns maintained their habits and diet routine, but their meals were supplemented with 500 mL/d of alcohol-free beer (0.0%) divided into two doses over a 45-d period. Lipid profile, inflammatory markers such as C-reactive protein, interleukins 1 and 6, and tumor necrosis factor-alpha, and parameters of oxidative metabolism were determined before and after the study period.
There were no differences in the levels of C-reactive protein and proinflammatory cytokines after diet supplementation. The antibody titers to oxidized low-density lipoprotein were significant lower (P < 0.05), and thiobarbituric acid-reactive substances (-18%, P < 0.001) and plasma carbonyl group content (-21%, P < 0.001) were decreased when compared with initial values. Increases in alpha-tocopherol levels (+9%, P < 0.05) and erythrocytic glutathione levels (+29%, P < 0.001) were also noted. With respect to lipid profile, only subjects with cholesterol levels higher than 240 mg/dL showed lower levels after supplementation.
Consumption of non-alcoholic beer produces a decrease in oxidative stress that can have a beneficial impact on cardiovascular risk; however, the circulating concentrations of inflammatory mediators involved in its pathophysiology remained unchanged.
... Two of these studies were carried out in nuns, a very interesting population because, due to their lifestyle, it is more homogeneous than other population groups (Table 1). The study published by Martinez- Alvarez et al. (2009) was carried out in 29 postmenopausal nuns (a population particularly at risk for atherosclerotic disease), aged 58-73 years [10]. They were given two 250 mL/day non-alcoholic lager beers with normal daily meals, for 45 days. ...
... Two of these studies were carried out in nuns, a very interesting population because, due to their lifestyle, it is more homogeneous than other population groups (Table 1). The study published by Martinez- Alvarez et al. (2009) was carried out in 29 postmenopausal nuns (a population particularly at risk for atherosclerotic disease), aged 58-73 years [10]. They were given two 250 mL/day non-alcoholic lager beers with normal daily meals, for 45 days. ...
... However, in other studies addressing subjects (men and women) who were overweight or obese without other cardiovascular risk factors, no significant effects were found [15,23]. Regarding non-alcoholic beer, only one of the studies included in this review found an increase in HDL-cholesterol [10]. Likely, ethanol contained in conventional beer is involved in the positive effect of this type of beer but, according to the results published, the influence of polyphenols cannot be discarded. ...
Numerous studies have revealed the beneficial effects of moderate beer consumption on cardiovascular diseases. However, the presence of alcohol in beer can represent a matter of concern, since alcohol intake poses a risk to some individuals. Additionally, adults who are life-long abstainers should not be encouraged to consume alcohol for health purposes. Consequently, the benefits of beer consumption remain a controversial issue. In this scenario, the present review gathers the reported information concerning the cardiovascular effects of non-alcoholic beer, and makes a comparison between these effects and those of conventional beer. Despite the scarcity of published results to date describing the effects of non-alcoholic beer consumption, the available literature indicates that it is more effective than conventional beer in preventing oxidative stress (lower lipid and protein oxidation), preserving the endothelial function (lower endothelial dysfunction) and inhibiting thrombogenic activity (lowered oxidized LDL). By contrast, conventional beer has shown to induce greater increases in HDL-cholesterol levels (known as a cardiovascular protective factor) compared to non-alcoholic beer. This effect cannot be solely attributed to alcohol content, since the polyphenol content in conventional beer tends to be higher than that found in non-alcoholic beer.
... The alcohol-free drink additionally reduced systolic, but not diastolic blood pressure compared to the other beverages [49]. Alcohol-free beer, in a single arm study of 29 nuns aged 53-73 years for 45 days, did not decrease markers of inflammation but reduced oxidized LDL cholesterol and increased glutathione levels, suggesting an enhanced antioxidant capacity to potentially reduce the risk of cardiovascular risk [50]. Additional work investigating the effect of dealcoholized beer on hemostasis, which was part funded by the brewer, in 12 young men, showed it to reduce both PAI activity and Factor VII coagulant activity, which could potentially reduce the risk of atherosclerotic disease, at least in the short term [51]. ...
... As of February 2020, a search of the World Health Organisation (WHO) Clinical Trial Registry (https://www.who.int/en/) identified eight registered clinical trials, of which only three have been published, two have been included in this review [49][50][51][52] and the third is related to bowel function, which was not within the scope of this review. ...
Beer is a beverage of significant historical and cultural importance. Interest in the potential health effects of alcoholic beverages has largely focused on wine; however, there are a number of potentially beneficial bioactives that beer may contain that warrant further investigation. The challenge of considering any potential health benefits of beer are restricted by the negative consequences of its alcohol and energy content. There is potential to enhance the bioactive qualities of beer whilst reducing the alcohol and energy content through novel brewing approaches often used in craft brewing, in terms of ingredients, brewing methods and type of fermentation. Consumer demand to produce a greater variety of beer types, including alcohol-free beers, may also help to increase the number of beers which may have greater potential to improve health, with lower levels of alcohol, while still being tasty products. As low alcohol, prebiotic and bioactive containing beers are developed, it is important that their potential health benefits and risks are fully assessed.
... Potential mechanisms of protective effects of beer in cardiovascular system have been studied [119][120][121]. An in vivo study reported that light to moderate beer drinking (12.5-25 g/day) could also improve endothelial function through inhibiting vascular oxidative damage and modulating the Akt/endothelial NO synthase pathway, which should be attributed to the non-alcohol components in beer [119]. ...
... According to a randomized crossover trial in high cardiovascular male volunteers, the phenolic components in beer (660 mL/day, contained 30 g alcohol for 4 weeks) provided additional protective effects compared to alcohol alone through downregulating the leukocyte adhesion molecules and inflammatory biomarkers in serum [120]. In addition, an intervention study reported that, consumption of non-alcoholic beer (500 mL/day) among post-menopausal women led to reduced oxidative stress which might be beneficial to the cardiovascular system [121]. ...
Epidemiological and experimental studies have consistently linked alcoholic beverage consumption with the development of several chronic disorders, such as cancer, cardiovascular diseases, diabetes mellitus and obesity. The impact of drinking is usually dose-dependent, and light to moderate drinking tends to lower risks of certain diseases, while heavy drinking tends to increase the risks. Besides, other factors such as drinking frequency, genetic susceptibility, smoking, diet, and hormone status can modify the association. The amount of ethanol in alcoholic beverages is the determining factor in most cases, and beverage types could also make an influence. This review summarizes recent studies on alcoholic beverage consumption and several chronic diseases, trying to assess the effects of different drinking patterns, beverage types, interaction with other risk factors, and provide mechanistic explanations.
... Furthermore, studies using alcohol-free beer also found beneficial effects on markers associated with liver health (i.e. markers of lipid peroxidation) (Martinez Alvarez et al., 2009). In a recent study of our own group we found that in female mice, shown to be more susceptible to alcohol-induced liver damage, the damaging effects of beer on the liver were less pronounced when compared to equal doses of plain ethanol (Kanuri et al., 2014); however, molecular mechanisms underlying this less damaging effect of beer on the liver but also eventual gender-specific differences have not been clarified yet. ...
... It has further been shown that chronic intake of elevated amounts of beer and wine in comparison to spirits may have less harmful effects on the liver (Kerr et al., 2000;Ponicki and Gruenewald, 2006). The results of others (Martinez Alvarez et al., 2009) even suggest that alcohol-free beer may have beneficial effects on lipid profile and pro-inflammatory markers related to liver diseases. It was further shown that some beer constituents like xanthohumol might have inhibitory effects on hepatic inflammation and fibrosis (Van et al., 2009;Dorn et al., 2012). ...
Mechanisms involved in the less damaging effects of beer in comparison to hard spirits have not yet been fully understood. The aim of the study was to determine if the effect of beer intake on the liver differs from that of plain ethanol and if so to determine mechanisms involved.
Male C57BL/6J mice received either ethanol, beer (ethanol content: 6 g/kg body weight) or iso-caloric maltodextrin solution. Markers of steatosis, lipogenesis, activation of the toll-like receptor-4 signaling cascade and lipid export in liver and tight junction proteins in duodenum were measured 6 and 12 h after acute ethanol or beer intake.
Alcohol ingestion resulted in a significant increase of hepatic triglyceride accumulation 6 and 12 h after ingestion, respectively, being markedly lower in mice fed beer. Expression of sterol regulatory element-binding protein-1c mRNA was significantly lower 12 h after alcohol or beer exposure, while fatty acid synthase mRNA expression was induced in livers of ethanol-fed mice and to a lesser extent in mice fed beer 6 h after acute alcohol ingestion. Protein levels of tight junction proteins in the small intestine were similar between groups while expression of myeloid differentiation primary response gene 88 in livers was significantly induced in ethanol- but not in beer-fed mice. Concentrations of 4-hydroxynonenal protein adducts and inducible nitric oxide synthase protein were also only induced in livers of mice fed ethanol. Protein levels of apolipoprotein B were induced in livers of beer-fed mice only.
Our data suggest that beer is less harmful on the development of acute alcohol-induced liver damage than plain ethanol in male mice.
© The Author 2015. Medical Council on Alcohol and Oxford University Press. All rights reserved.
... A 45-day study of postmenopausal women consuming 500 mL of non-alcoholic beer per day found that intake of non-alcoholic beer lowered cholesterol levels in subjects with blood cholesterol greater than 240 mg/dL (58), which supports the role of long-term non-alcoholic beer consumption in combating mild chronic inflammation and preventing metabolic disorders. Similarly, supplementing mothers' diets with non-alcoholic beer reduced oxidative damage in lactating mothers, thereby increasing the antioxidant capacity of breast milk (32). ...
As a long-established fermented beverage, beer is rich in many essential amino acids, vitamins, trace elements, and bioactive substances that are involved in the regulation of many human physiological functions. The polyphenols in the malt and hops of beer are also important active compounds that interact in both directions with the gut microbiome. This review summarizes the mechanisms by which polyphenols, fiber, and other beneficial components of beer are fermentatively broken down by the intestinal microbiome to initiate the mucosal immune barrier and thus participate in immune regulation. Beer degradation products have anti-inflammatory, anticoagulant, antioxidant, and glucolipid metabolism-modulating potential. We have categorized and summarized reported data on changes in disease indicators and in vivo gut microbiota abundance following alcoholic and non-alcoholic beer consumption. The positive effects of bioactive substances in beer in cancer prevention, reduction of cardiovascular events, and modulation of metabolic syndrome make it one of the candidates for microecological modulators.
... Only studies on cardiovascular diseases and with incomplete designs were found, such as Bassus et al. (2004) who examined 12 subjects (only men) and the intervention only lasted 3 h; they did not mention the type of study, standardization and monitoring of lifestyle or diet during the intervention. Alvarez et al. (2009a) only included female participants, did not mention age range or standardization of lifestyle or diet before the intervention, and only included non-alcoholic beers as samples. The range of duration between studies was from 3 h to 45 days and although the lifestyle or diet during the intervention was standardized, the nature of the study limits the control of environmental conditions, which would lead to inconclusive results. ...
Currently, there is greater production and consumption of craft beer due to its appreciated sensory characteristics. Unlike conventional beer, craft beers provide better health benefits due to their varied and high content of phenolic compounds (PCs) and also due to their alcohol content, but the latter is controversial. The purpose of this paper was to report on the alcoholic fraction and PCs present in craft beers and their influence on health. Despite the craft beer boom, there are few studies on the topic; there is a lot of field to explore. The countries with the most research are the United States > Italy > Brazil > United Kingdom > Spain. The type and amount of PCs in craft beers depends on the ingredients and strains used, as well as the brewing process. It was determined that it is healthier to be a moderate consumer of alcohol than to be a teetotaler or heavy drinker. Thus, studies in vitro, with animal models and clinical trials on cardiovascular and neurodegenerative diseases, cancer, diabetes and obesity, osteoporosis and even the immune system suggest the consumption of craft beer. However, more studies with more robust designs are required to obtain more generalizable and conclusive results. Finally, some challenges in the production of craft beer were detailed and some alternative solutions were mentioned.
... In the short term, 30 min after consumption, beer decreased the cytotoxic activity of peripheral lymphocytes stimulated with IL-2 or phytohemagglutinin of healthy subjects [86]; this would seem like a detrimental role of beer consumption on the immune response immediately after ingestion, nevertheless, blood lymphocytes were more resistant to radiation-induced damage from 30 min to 4.5 h after beer ingestion [87]; this could be beneficial in the case of cancer patients receiving radiotherapy. Moderate (330 mL for women, 660 mL for men) beer consumption in healthy subjects did not affect the serum levels of the adhesion molecules ICAM-1 and E-selectin [88] nor the levels of cytokines or complement proteins involved in the serum immune response [90]. Moreover, as part of a study to determine the effect of moderate beer consumption on immunocompetence in healthy adults, sixty subjects (29 women and 31 men) between 25 and 50 years consumed, after a month of abstinence, one or two cans of beer as part of a regular diet during a month. ...
Beer is a fermented beverage widely consumed worldwide with high nutritional and biological value due to its bioactive components. It has been described that both alcoholic and non-alcoholic beer have several nutrients derived from their ingredients including vitamins, minerals, proteins, carbohydrates, and antioxidants that make beer a potential functional supplement. Some of these compounds possess redox, anti-inflammatory and anticarcinogenic properties making the benefits of moderate beer consumption an attractive way to improve human health. Specifically, the hop cones used for beer brewing provide essential oils, bitter acids and flavonoids that are potent antioxidants and immune response modulators. This review focuses on the redox and anti-inflammatory properties of hop derivatives and summarizes the current knowledge of their neuroprotective effects.
... Even though the non-alcoholic beer has a lower concentration of phenol compounds and antioxidant activity than regular beers, its moderate amount of calorie content gives rise to the growing consumption of this beverage in recent years (Müller et al. 2016). On the whole, non-alcoholic beer, the same as the regular one, has a lot of bioactive compounds (Alvarez et al. 2009;De Gaetano et al. 2016). Indeed, depending on the production technique and the raw materials, beer has a different composition (Yalçınçıray et al. 2020). ...
This paper seeks to evaluate the quantity of B1, B2 and B6 vitamins using HPLC method and investigate the amount of total phenolic content (TPC), total flavonoid content (TFC) and DPPH radical scavenging activity (antioxidant activity), pH, Brix and color of Iranian non-alcoholic beers. For doing so, four bottles of non-alcoholic beer (named from A to D) purchased from Iranian markets were investigated over a three-month storage period. Results demonstrated that after the storage time, TPC, TFC and antioxidant activity of all the samples reduced noticeably. Sample B had the highest level of total phenolic content, which was 10.17 mg of GAE/mL, but it had the lowest antioxidant activity showing the higher responsibility of the type of phenolic compounds in antioxidant activity than their quantity. Moreover, the results of HPLC method, conducted in the third month, showed that sample B had the highest level of vitamin B1 and B6, which were 68.47 and 43.11 mg/kg, respectively. In addition, vitamin B1 had the highest amounts in both samples. According to the results, it can be said that Iranian non-alcoholic beers contain a significant amount of total phenolic, flavonoid compounds with high antioxidant activity and B vitamins.
... In another similar, but a crossover, acute intervention of beer or wine (or vodka for the evaluation of the contribution of alcohol) inhibition of oxidative stress induced (by 100% normobaric O 2 breathing) was tested [106]. Analysis of stiffness (500 mL) for 45 days to postmenopausal women (n = 29) was associated with a reduction of several indicators of early protein oxidation, especially reducing cholesterol levels in subjects with higher than 240 mg/dL [108], supporting the usefulness of long-term alcohol-free beer consumption in fighting low-grade chronic inflammation and preventing metabolic disorders. As an alcoholic beer was not tested, one might speculate that alcohol can abolish the beneficial effect. ...
This review reports recent knowledge on the role of ingredients (barley, hop and yeasts), including genetic factors, on the final yield of phenolic compounds in beer, and how these molecules generally affect resulting beer attributes, focusing mainly on new attempts at the enrichment of beer phenols, with fruits or cereals other than barley. An entire section is dedicated to health-related effects, analyzing the degree up to which studies, investigating phenols-related health effects of beer, have appropriately considered the contribution of alcohol (pure or spirits) intake. For such purpose, we searched Scopus.com for any kind of experimental model (in vitro, animal, human observational or intervention) using beer and considering phenols. Overall, data reported so far support the existence of the somehow additive or synergistic effects of phenols and ethanol present in beer. However, findings are inconclusive and thus deserve further animal and human studies.
... A few years ago, NAB consumption was evaluated for its effect in atherosclerosis-related factors such as lipid profile, oxidative stress parameters, and proinflammatory cytokines in 29 postmenopausal women. Thus, a study published in 2009 indicated that the consumption of NAB 0% ABV (500 mL/45 days) results in decreased oxidative stress with a potentially positive impact on a cardiovascular level [129]. Finally, NAB can be included in one's diet for its preventive action in diseases related to oxidative stress; however, further clinical studies are needed to illustrate the long-term effects on cardiovascular disease from regular NAB consumption. ...
Consumers' demand for functional fermented food that can fulfill nutritional needs and help maintain a balanced diet while also having a positive impact on one's health status is increasing all over the world. Thus, healthy choices could include beverages with nutrients and bioactive compounds which can be used as an effective disease-prevention strategy. Regular beer has certain health benefits which inspire further research with the prospect of obtaining special functional beers with little or no alcohol content. As observed, the special beer market remains highly dynamic and is predicted to expand even further. Therefore, brewers need to keep up with the consumers' interests and needs while designing special beers, namely nonalcoholic beers (NABs), low-alcohol beers (LABs), and craft beers (CBs). Thus, understanding the potential uses of bioactive compounds in special beer, the wide range of therapeutic effects, and the possible mechanisms of action is essential for developing healthier beverages. This review aimed to evaluate the nutritional features of special beers, and their proven or potential beneficial actions on one's health status and in preventing certain diseases.
... In these studies, the less damaging effects of beer were associated with a protection against the induction of toll-like receptor (TLR)-4-and inducible nitric oxide synthase-(iNOS) dependent signaling cascades in the liver. In line with these findings, results obtained in human intervention studies using alcohol-free beer suggest that regular intake of alcohol-free beer can promote anti-oxidative capacity (Franco et al., 2013) and is associated with improved lipid profiles but also lower markers of oxidative stress in elderly women (Martinez Alvarez et al., 2009). Furthermore, consumption of alcohol-free beer protected rats from adriamycin-induced heart and liver toxicity due to a reduction of markers of lipid peroxidation in the liver (Valls-Belles et al., 2008). ...
Aim
Using a binge-drinking mouse model, we aimed to determine whether hops (Humulus lupulus) in beer is involved in the less damaging effects of acute beer consumption on the liver in comparison with ethanol.
Methods
Female C57BL/6 J mice were either fed one iso-alcoholic and iso-caloric bolus dose of ethanol, beer, beer without hops (6 g ethanol/kg body weight) or an iso-caloric bolus of maltodextrin control solution. Markers of steatosis, intestinal barrier function, activation of toll-like receptor 4 signaling cascades, lipid peroxidation and lipogenesis were determined in liver, small intestine and plasma 2 h and 12 h after acute alcohol ingestion.
Results
Alcohol-induced hepatic fat accumulation was significantly attenuated in mice fed beer whereas in those fed beer without hops, hepatic fat accumulation was similar to that found in ethanol-fed mice. While markers of intestinal barrier function e.g. portal endotoxin levels and lipogenesis only differed slightly between groups, hepatic concentrations of myeloid differentiation primary response gene 88, inducible nitric oxide synthase (iNOS) and plasminogen-activator inhibitor 1 protein as well as of 4-hydroxynonenal and 3-nitrotyrosine protein adducts were similarly elevated in livers of mice fed ethanol or beer without hops when compared with controls. Induction of these markers was markedly attenuated in mice fed hops-containing beer.
Conclusion
Taken together, our data suggest that hops in beer markedly attenuated acute alcohol-induced liver steatosis in female mice through mechanisms involving a suppression of iNOS induction in the liver.
... After the alcohol-free beer period, oxidized LDL, thiobarbituric acid-reactive substances (TBARS) and plasma carbonyl group content decreased. In addition, alpha-tocopherol levels and erythrocyte glutathione levels increased, showing a cardioprotective antioxidant effect of alcoholfree beer consumption [138]. ...
A large evidence-based review on the effects of a moderate consumption of beer on human health has been conducted by an international panel of experts who reached a full consensus on the present document.
... Anti-inflammatory effects have also been shown with other alcoholic beverages (26,27). One recent study (28) oxidative stress, but no change in inflammatory markers with alcohol-free beer in elderly women, supporting the active effects of alcohol. Alcohol with a high glycemic index (GI) meal can reduce the post-prandial response to that meal (15), and moderate intake is associated with reduced glucose levels in diabetics (29) -even those who are normally non-drinkers (30). ...
The discovery of a form of low-grade systemic inflammation (called 'metaflamma-tion'), and the close evolutionary link between the immune and metabolic systems, poses questions about the supposed antigens (inducers) of such an immune reaction. Initially, this was thought to be mediated through obesity. However, we have identified a number of lifestyle or environmentally related inducers that may cause metaflammation, even in the absence of obesity. In this paper, the third of a series linking obesity with broad environmental and evolutionary factors, we identify nutritional stimuli with evidence of an involvement in metaflammation. From this we propose that components of certain foods and beverages with which humans have not evolved, are more often the inducers of an inflammatory effect in the body than those with which humans have become more familiar, and to which a neutral, or anti-inflammatory response may be expected to have developed. The implications of such a finding are considered in relation to broader aspects of the environment, economic growth, policy change and current global financial issues.
... Podobne wyniki otrzymali Alvarez i wsp. [33] nie stwierdzili oni u zdrowych osób, w porównaniu z grupą kontrolną, różnic w poziomie IL-6 w osoczu po 45-dniowym okresie spożywania piwa bezalkoholowego (0,5 litra dziennie). Inni autorzy podkreślają, że ważna jest ilość spożywanego alkoholu, gdyż jego umiarkowane ilości mogą oddziaływać korzystnie. ...
Introduction: Excessive alcohol intake can directly inhibit the immune response. Ethyl alcohol affects changes of plasma cytokine concentrations and in various tissues disturbs the balance between the multifunctional proteins that play a pivotal role in immunological and inflammatory responses. The aim of this study was to evaluate the effect of beer or ethanol consumption on selected plasma cytokine concentrations in young male rats.
Material and methods: The experiment was conducted on 30-day old male Wistar rats divided into 4 groups (B2, B6, E2, and E6) and 2 control groups (C2 and C6). Rats from B2 and B6 groups were exposed to beer (10% of ethanol), and those from E2 and E6 groups to 10% ethanol solution for 2 or 6 weeks respectively. The rats had free access to alcohol and lab chow, but water was supplied during the photoperiod light phase. The rats were anesthetised after two or six weeks of the experiment and the blood was sampled by heart puncture and collected into heparinised tubes. Plasma IL-6 and IL-10 concentrations were measured using ELISA kits.
Results: Statistical analysis has shown that plasma IL-10 concentration was significantly increased in E6 versus C6 and E2 groups of rats. Decreased plasma IL-6 concentration in E2 in comparison with C2 group of rats was also found. At the same time, significantly higher IL-6 concentration was observed in B6 versus C6 and E6 groups.
Our results indicate disruption of cytokine production, which may impair immunological defence and influence proinflammatory reactions.
... Red wine, for example, has consistently been reported to have anti-inflammatory effects [162], leading to speculation that these effects may simply be derived from grape-derived antioxidants in the wine. However, other alcoholic beverages such as beer and liquor have also been found to have anti-inflammatory properties [163]. Overall, this implicates small doses of alcohol to be anti-inflammatory. ...
Research examining immune function during obesity suggests that excessive adiposity is linked to impaired immune responses leading to pathology. The deleterious effects of obesity on immunity have been associated with the systemic proinflammatory profile generated by the secretory molecules derived from adipose cells. These include inflammatory peptides, such as TNF- α , CRP, and IL-6. Consequently, obesity is now characterized as a state of chronic low-grade systemic inflammation, a condition considerably linked to the development of comorbidity. Given the critical role of adipose tissue in the inflammatory process, especially in obese individuals, it becomes an important clinical objective to identify lifestyle factors that may affect the obesity-immune system relationship. For instance, stress, physical activity, and nutrition have each shown to be a significant lifestyle factor influencing the inflammatory profile associated with the state of obesity. Therefore, the purpose of this review is to comprehensively evaluate the impact of lifestyle factors, in particular psychological stress, physical activity, and nutrition, on obesity-related immune function with specific focus on inflammation.
... It has recently been shown that non-alcoholic beer retains much of the antioxidant content attributed to polyphenols without the adverse effects of an alcoholic drink. 13,14 However, little is known about the influence of non-alcoholic beer consumption in lactating women and in their breastmilk. ...
Background:
After delivery and birth, mothers and neonates are exposed to oxidative stress. We tested whether supplementing the diet of breastfeeding mothers with non-alcoholic beer, a product rich in antioxidants, could improve their oxidative status and the antioxidant content of their milk. A prospective trial begun on Day 2 postpartum was conducted in mother-infant dyads.
Subjects and methods:
Sixty breastfeeding mothers and their infants were allocated to either a control group (n=30) on a free diet or a study group (n=30) on a free diet supplemented with 660 mL of non-alcoholic beer/day. The oxidative status of the mothers' breastmilk, plasma, and urine and the infant's urine was analyzed on Days 2 and 30 postpartum. The before-after difference was compared within and between the groups.
Results:
The increase in antioxidant capacity and coenzyme Q10 content in the breastmilk of the study group at Day 30 was higher than in that of the control group (p<0.001). There was also a change in the oxidative status of the mothers' plasma in the supplemented group regarding the control group; higher values of total antioxidant capacity (p<0.05) and lower levels of 8-hydroxydeoxyguanosine (p<0.05), indicative of DNA oxidative damage, were found. These results indicate a positive effect of non-alcoholic beer supplementation on oxidative stress in mothers. However, no difference in oxidant markers was found in the infant's urine.
Conclusions:
The consumption of non-alcoholic beer appears to enhance the antioxidant capacity of breastmilk and decrease oxidative damage in breastfeeding mothers.
... Up to date, several studies have confirmed beneficial cardiovascular effects of moderate and daily consumption of fermented beverages (wine and beer) in populations consuming the healthy Mediterranean diet. Indeed, a U-shaped association between drinking and the incidence of CHD has been repeatedly reported [32] The increase in HDL has been postulated to be one of the mechanisms whereby alcohol per se benefits the heart since free-alcohol beverage consumption has shown to exert no changes in lipid profile [28]. Apart from the well-known ability of HDL to eliminate cholesterol from the vessels by reverse cholesterol transport, HDL and its constituent sphingosine-1-phosphate (S1P) [40] have shown to acutely protect the heart against I/R injury in vivo by inhibiting inflammatory cell recruitment and cardiomyocytes apoptosis [12,47]. ...
Mild-to-moderate alcohol consumption has been associated with reduced risk of morbi/mortality from coronary artery disease. However, whether beer intake affords cardioprotection remains unclear. We investigated whether beer intake (alcohol-containing and alcohol-free brew) provides cardioprotection in a pig model of myocardial infarction (MI). Pigs were randomly assigned to: (1) be fed for 10 days a high-cholesterol diet (HC); (2) HC + low-dose beer (LB; 12.5 g alcohol/day); (3) HC + moderate-dose beer (MB; 25 g alcohol/day); or IV) HC + alcohol-free-MB (0.0 g alcohol/day) before MI induction and kept 21 days with the same regime. Scar size, echocardiography, biochemical and oxidative parameters were assessed. Myocardial tissue was obtained for molecular analysis and histology. All beer-fed animals were less prone to arrhythmogenesis during ischemia. At sacrifice, beer intake was associated with lower oxidative stress and higher HDL-antioxidant capacity. Within the ischemic myocardium beer-fed animals showed higher Akt/eNOS and AMPK activation and reduced sirtuin1-related apoptosis. Compared to controls beer intake was associated with lower lipid infiltration, higher TGFβ-related collagen fibril formation and diminished MMP9 activity in the fibrous tissue limiting scar size (HC + LB and HC + MB P < 0.05 and HC + alcohol-free-MB P = 0.068 vs. HC). Systolic-related parameters were similarly worsen post-MI in all groups and further deteriorated in control animals (P ≤ 0.05 vs. post-MI). At sacrifice, all animals showed a worsening in diastolic-related parameters but overall cardiac performance was improved in beer-fed animals regardless of the dose or alcohol content (P ≤ 0.05). In conclusion, beer intake reduces oxidative stress and apoptosis, activates RISK components and favors reparative fibrosis improving global cardiac performance.
... The concentration of CySS, which is a covariable with E h CySS, is also increased in association with TNF-a [29], endothelial dysfunction [7], and increased carotid intima media thickness [6]. In addition, substantial literature shows that dietary inducers can affect tissue levels of GSH and related metabolites [31]. Thus, there is a need to understand dietary factors that affect plasma E h GSSG, E h CySS, or CySS concentration in humans. ...
Oxidation of plasma cysteine/cystine (Cys/CySS) redox potential (E(h)CySS) has been associated with risk factors for cardiovascular disease in humans. Cys and CySS are derived from dietary sulfur amino acids (SAA), but the specific effects of SAA depletion and repletion on Cys/CySS redox indices are unknown. The present study examined the effect of dietary SAA intake level on free Cys, free CySS, and E(h)CySS in human plasma under fasting conditions.
Healthy individuals aged 18-36 y (n = 13) were equilibrated to foods providing the RDA for SAA and then fed chemically defined diets without SAA (0 mg · kg(-1) · d(-1); n = 13) followed by SAA at levels approximating the mean (56 mg · kg(-1) · d(-1); n = 8) or 99th percentile (117 mg · kg(-1) · d(-1); n = 5) intake levels of Americans. Fasting plasma samples were collected daily during 4-d study periods and analyzed for free Cys, free CySS, and the E(h)CySS.
The SAA-free diet significantly (P < 0.05) decreased plasma-free Cys concentrations and oxidized E(h)CySS values after 4 d of SAA depletion. With SAA repletion at 56 mg · kg(-1) · d(-1), plasma-free Cys increased significantly and values for E(h)CySS became more reduced. Administration of a diet providing a higher dose of SAA (117 mg · kg(-1) · d(-1)) resulted in a significantly higher level of free Cys and a more reduced E(h)CySS.
These results show that free Cys and Cys/CySS redox potential (E(h)CySS) in fasting plasma are affected by dietary SAA intake level in humans. Significant changes occur slowly over 4 d with insufficient SAA intake, but rapidly (after 1 d) with repletion.
... Anti-inflammatory effects have also been shown with other alcoholic beverages (26,27). One recent study (28) oxidative stress, but no change in inflammatory markers with alcohol-free beer in elderly women, supporting the active effects of alcohol. Alcohol with a high glycemic index (GI) meal can reduce the post-prandial response to that meal (15), and moderate intake is associated with reduced glucose levels in diabetics (29) -even those who are normally non-drinkers (30). ...
The discovery of a form of low-grade systemic inflammation (called 'metaflammation'), and the close evolutionary link between the immune and metabolic systems, poses questions about the supposed antigens (inducers) of such an immune reaction. Initially, this was thought to be mediated through obesity. However, we have identified a number of lifestyle or environmentally related inducers that may cause metaflammation, even in the absence of obesity. In this paper, the third of a series linking obesity with broad environmental and evolutionary factors, we identify nutritional stimuli with evidence of an involvement in metaflammation. From this we propose that components of certain foods and beverages with which humans have not evolved, are more often the inducers of an inflammatory effect in the body than those with which humans have become more familiar, and to which a neutral, or anti-inflammatory response may be expected to have developed. The implications of such a finding are considered in relation to broader aspects of the environment, economic growth, policy change and current global financial issues.
Experimental and clinical studies evidenced the health effects of moderate consumption of beer, mainly due to the presence of bioactive compounds, such as polyphenols, vitamins, or fibers. To exploit the potential beneficial effect on health and in disease prevention of these compounds, a new beverage based on barley malts and hops named Aliophen® has been designed, through a patented production process, with a high total polyphenolic amount compared to alcohol-free beer and similar to the one present in light and dark beers. In the present study, the antioxidant activity of Aliophen® against low-density lipoprotein (LDL) oxidation and its ability to protect erythrocytes from hemolysis have been characterized. Moreover, the chemopreventive effect of Aliophen® against colon cancer has been assessed, employing a mouse model of chemically induced carcinogenesis using azoxymethane (AOM). Data obtained showed that Aliophen at a low dose (3 mg/kg) inhibited the formation of preneoplastic lesions, polyps, and tumors. At higher doses (300 mg/kg) the protective effect was measured in the first phase of the onset of cancer. The antioxidant properties of Aliophen® were also observed in AOM-treated mice where it increased the serum antioxidant capacity. Based on the data presented, Aliophen® can exert promising health effects, including an anticancer capacity presumably associated with its antioxidant properties.
Age, sex and diet are well-established risk factors for several diseases. In humans, each of these variables has been linked to differences in plasma redox potentials (Eh) of the glutathione/glutathione disulfide (GSH/GSSG) and cysteine/cystine (Cys/CySS) redox couples. Mice have been very useful for modeling human disease processes, but it is unknown if age, sex and diet affect redox couples in mice as they do in humans. The purpose of the present study was to examine the effects of these factors on plasma redox potentials in C57BL/6 J mice. We found that age had no effect on either redox couple in either sex. Plasma Eh Cys/CySS and Eh GSH/GSSG were both more oxidized (more positive) in females than in males. A 24-h fast negated the sex differences in both redox potentials by oxidizing both redox couples in male mice, while having no effect on Eh Cys/CySS and a smaller effect on Eh GSH/GSSG in female mice. A diet with excess sulfur amino acids reduced the plasma Eh Cys/CySS in females to a level comparable to that seen in male mice. Thus, sex-specific differences in plasma Eh Cys/CySS could be normalized by two different dietary interventions. Some of these findings are consistent with reported human studies, while others are not. Most strikingly, mice do not exhibit age-dependent oxidation of plasma redox potentials. Care must be taken when designing and interpreting mouse studies to investigate redox regulation in humans.
Background & aims:
The quality of carbohydrates has an essential role in nutritional management of type 2 diabetes mellitus (T2DM) because of its substantial impact on glucose homeostasis. Alcohol-free beer has beneficial bioactive components but it has a relatively high glycemic-index so its consumption is restricted in diabetic subjects. We aimed to explore the effect of an alcohol-free beer with modified carbohydrate composition almost completely eliminating maltose and adding isomaltulose (16.5 g/day) and a resistant maltodextrin (5.28 g/day) in comparison to a regular alcohol-free beer on glycemic control of diabetic subjects with overweight or obesity.
Design:
We randomized 41 subjects into two groups: a) consumption of 66 cL/day of; regular alcohol-free beer for the first 10 weeks and 66 cL/day of alcohol-free beer with modified carbohydrate composition for the next 10 weeks; b) the same described intervention in opposite order. There was a washout period for 6-8 weeks between the two interventions. Participants were counseled to adhere to a healthy diet for cardiovascular health and to increase physical activity. Clinical, biochemical, anthropometric, lifestyle and satiety assessments were performed at the beginning and at the end of each period.
Results:
Subjects showed significantly weight loss after the two ten weeks periods (-1.69 ± 3.21% and -1.77 ± 3.70% after experimental and regular alcohol-free beers, respectively, P = 0.881). Glucose and glycated hemoglobin did not significantly change after any period. Insulin concentrations and HOMA-IR significantly decreased (-11.1 [-21.3-4.64]% and -1.92 ± 32.8% respectively) after the intake of experimental alcohol-free beer but not after regular alcohol-free beer. Reductions remained statistically significant after adjusting for weight loss, energy intake, physical activity and intervention order. Subjects reported higher satiety scores after consuming experimental alcohol-free beer.
Conclusions:
An alcohol-free beer including the substitution of regular carbohydrates for low doses of isomaltulose and the addition of a resistant maltodextrin within meals led to an improvement in insulin resistance in subjects with T2DM and overweight or obesity.
Clinical trial registration:
The clinical trial has been registered in ClinicalTrials.gov (Identifier: NCT03337828).
Membrane-based and thermal methods to produce non-alcoholic beverages have been used for many years to remove ethanol from beer and other alcoholic, fermented matrices. The aim of all applied methods is to eliminate the ethanol as selectively as possible. Besides legal regulations and nutritional health benefits, different physical production methods as well as the effects on the aroma composition after different production steps and possibilities for procedural descriptions are elucidated.
In this study 40 Hungarian retail beers were evaluated for folic acid content, antioxidant profile and physicochemical parameters. The physicochemical parameters, folic acid content and antioxidant activity of alcohol-free beers were the lowest. Folic acid content of beers aged with sour cherries showed high values, more than 0.4 mg/l and an alcohol-free beer-based mixed drink made with lemon juice contained more than 0.2 mg/l of folic acid. Dark beers and beers aged with sour cherries had the highest antioxidant activity probably owing to their high extract content, components released from the fruits and special malts. These results highlight the possibility of achieving adequate folic acid and relevant antioxidant intake without excessive alcohol and energy consumption by selecting appropriate beer types.
de Membranbasierte und thermische Verfahren werden seit vielen Jahren zur Herstellung alkoholfreier Getränke genutzt, um Ethanol aus Bier oder anderen alkoholhaltigen, fermentierten Matrizes zu entfernen. Ziel ist, Ethanol möglichst selektiv und unter Berücksichtigung der Verluste wertgebender Aromastoffe zu entziehen. Neben gesetzlichen Grundlagen und gesundheitsrelevanten Aspekten werden verschiedene Technologien sowie deren Auswirkungen auf die Aromastoffzusammensetzung von Zwischen‐ und Endprodukten erläutert. Auch auf die Möglichkeiten zur verfahrenstechnischen Beurteilung thermischer Verfahren wird eingegangen.
Abstract
en Membrane‐based and thermal methods are used for many years, to produce alcohol‐free beverages by removing ethanol from beer and other alcoholic, fermented matrices. The aim of all applied methods is to eliminate the ethanol as selective as possible. Besides legal regulations and nutritional health benefits, different physical production methods plus the effects on the composition of aroma components after different production steps and possibilities for procedural descriptions, are elucidated.
Background:
There is controversy regarding the effect of alcohol beverage intake in vascular vasodilatory function in peripheral arteries. The effects of beer intake in coronary vasodilation remain unknown. We investigated whether regular beer intake (alcohol and alcohol-free) protects against hypercholesterolaemia-induced coronary endothelial dysfunction and the mechanisms behind this effect.
Materials and methods:
Pigs were fed 10 days: (i) a Western-type hypercholesterolaemic diet (WD); (ii) WD+low-dose beer (12·5 g alcohol/day); (iii) WD+moderate-dose beer (25 g alcohol/day); or (iv) WD+moderate-dose alcohol-free-beer (0·0 g alcohol/day). Coronary responses to endothelium-dependent vasoactive drugs (acetylcholine: receptor mediated; calcium ionophore-A23189: nonreceptor mediated), endothelium-independent vasoactive drug (SNP) and L-NMMA (NOS-antagonist) were evaluated in the LAD coronary artery by flow Doppler. Coronary Akt/eNOS activation, MCP-1 expression, oxidative DNA damage and superoxide production were assessed. Lipid profile, lipoproteins resistance to oxidation and urinary isoxanthohumol concentration were evaluated.
Results:
Alcoholic and nonalcoholic beer intake prevented WD-induced impairment of receptor- and non-receptor-operated endothelial-dependent coronary vasodilation. All animals displayed a similar vasodilatory response to SNP and L-NMMA blunted all endothelial-dependent vasorelaxation responses. Haemodynamic parameters remained unchanged. Coronary arteries showed lower DNA damage and increased Akt/eNOS axis activation in beer-fed animals. Animals taking beer showed HDL with higher antioxidant capacity, higher LDL resistance to oxidation and increased isoxanthohumol levels. Weight, lipids levels, liver enzymes and MCP-1 expression were not affected by beer intake.
Conclusions:
Non-alcoholic-related beer components protect against hyperlipemia-induced coronary endothelial dysfunction by counteracting vascular oxidative damage and preserving the Akt/eNOS pathway. Light-to-moderate beer consumption prevents and/or reduces the endothelial dysfunction associated with cardiovascular risk factors.
Purpose:
The aim of the present study was to assess whether the effects of acute consumption of stout or pilsner beer on the liver differ from those of plain ethanol in a mouse model.
Methods:
Seven-week-old female C57BL/6J mice received either ethanol, stout or pilsner beer (ethanol content: 6 g/kg body weight) or isocaloric maltodextrin solution. Plasma alanine transaminase, markers of steatosis, lipogenesis, activation of the toll-like receptor-4 signaling cascade as well as lipid peroxidation and fibrogenesis in the liver were measured 12 h after acute ethanol or beer intake.
Results:
Acute alcohol ingestion caused a marked ~11-fold increase in hepatic triglyceride accumulation in comparison to controls, whereas in mice exposed to stout and pilsner beer, hepatic triglyceride levels were increased only by ~6.5- and ~4-fold, respectively. mRNA expression of sterol regulatory element-binding protein 1c and fatty acid synthase in the liver did not differ between alcohol and beer groups. In contrast, expression of myeloid differentiation primary response gene 88, inducible nitric oxide synthases, but also the concentrations of 4-hydroxynonenal protein adducts, nuclear factor κB and plasminogen activator inhibitor-1 were induced in livers of ethanol treated mice but not in those exposed to the two beers.
Conclusion:
Taken together, our results suggest that acute ingestion of beer and herein especially of pilsner beer is less harmful to the liver than the ingestion of plain ethanol.
Combination of Opisthorchis viverrini infection and other factors could drive cholangiocarcinoma (CCA) development in Southeast Asia. However, other CCA factors are obscure. Alcohol consumption is well known in the risk for several cancers, but there is no report in CCA development. Therefore, the present study was to clarify whether drinking alcohol increases the liver pathology of Opisthorchis viverrini (OV) infection which may be the CCA risk. Experimental Syrian hamsters were divided into two groups: (1) infected with OV alone (OV); and (2) infected with OV plus administration of drinking alcohol (OV + ALC) for various lengths of time, i.e., 1, 2, 3, and 6 months. Hamster livers were collected for analysis of histopathological changes through hematoxylin and eosin, Sirius red, and immunohistostaining for proliferating cell nuclear antigen (PCNA) and cytokeratin 19 (CK19). Syrian hamster sera were used for liver function tests. Observed histopathological changes consisted primarily of aggregations of inflammatory cells surrounding the hepatic bile duct, especially at the hilar region, in both OV and OV + ALC groups; however, there was a difference in virulence. The OV + ALC group showed greater severity than the OV group. Moreover, in addition to aggregations of inflammatory cells, new bile duct formation (including hepatic cell death) was observed in subcapsular hepatic tissue. Bile duct proliferation, as determined by positive immunohistochemical staining for CK19 and PCNA, was correlated with the histopathology. Increased fibrosis was observed in subcapsular liver tissue. The present study suggests that alcohol consumption can exacerbate cholangiofibrosis, cholangitis, and lithiasis, which are risk factors for CCA.
Polyphenols exert beneficial effects in atherosclerosis. The crucial step in atherosclerosis is the recruitment of monocytes to the subendothelial space, induced by endothelial adhesion molecules through the activation of factors such as NF-κB. We studied the effect of a dealcoholised lager beer (DLB) and a dealcoholised dark beer (DDB) on atherosclerotic lesions, and the underlying mechanisms. Dealcoholised beers were administered in the diet (42 ml/kg body weight per d) to 4-week-old male apoE knockout (apoE − / − ) mice for 20 weeks. The atherosclerotic lesions in the thoracic aorta were reduced by 44 % (P = 0·003) and 51 % (P < 0·001) in DLB- and DDB-treated mice, respectively. Also, the mRNA expressions of the endothelial adhesion molecules in the total aorta were decreased: P-selectin showed a 17 % (P = 0·004) reduction in DDB-treated mice; vascular cell adhesion molecule-1 (VCAM-1) was decreased by 20 % (P = 0·012) and 32 % (P = 0·001) in DLB- and DDB-treated mice, respectively; intercellular adhesion molecule-1 (ICAM-1) showed a 14 % (P = 0·014) reduction in DLB-treated mice. The protein expressions of these molecules and NF-κB were studied in the aortic root. P-selectin was decreased by 37 % (P = 0·012) in DDB-treated mice; VCAM-1 was reduced by 48 % (P = 0·001) and 54 % (P < 0·001) in DLB- and DDB-treated mice, respectively; ICAM-1 was decreased by 25 % (P = 0·028) and 30 % (P = 0·018) in DLB- and DDB-treated mice, respectively; NF-κB was reduced by 46 % (P = 0·042) in DDB-treated mice. In conclusion, dealcoholised beers protected apoE − / − mice against atherosclerosis, through the modulation of endothelial adhesion molecules, possibly induced by NF-κB.
There is increasing evidence indicating that the dietary intake of food with high antioxidant capacity may protect mitochondria from damage and exert positive effects on different pathogenic processes.
The present study was designed to evaluate the possible protective effect of alcohol-free beer intake on chain components dysfunction of liver and heart mitochondria, and to compare with the effect of alcohol beer intake.
The study was carried out in rat heart and liver mitochondria by inducing with Adriamycin the dysfunction of the respiratory chain. Heart and liver mitochondria were isolated from rats and subjected to oxidative stress with two doses of Adriamycin (5 mg/Kg) 7 days from the beginning of consumption of both alcohol-free and alcohol beer during 31 days. Complexes I and IV and the levels of coenzymes Q(9) and Q(10) were evaluated and compared with a control group.
Liver and heart mitochondria isolated from rats treated with Adryamicin showed a decrease in levels of complex I and complex IV enzymatic activity and in levels of coenzymes Q(9) and Q(10). Beer intake for itself does not affect any of the studied parameters. Therefore, the consumption of both alcohol and alcohol-free beer by rats treated with Adriamycin prevents the inhibition of enzymatic activities of complexes I and IV and the oxidation of coenzymes Q(9) and Q(10) in rat heart and liver mitochondria.
These results indicate that alcohol-free beer prevents adriamycin-induced damage to mitochondrial chain components and, therefore, helps to prevent mitochondrial dysfunction.
Although moderate drinking confers a decreased risk of myocardial infarction, the roles of the drinking pattern and type of beverage remain unclear.
We studied the association of alcohol consumption with the risk of myocardial infarction among 38,077 male health professionals who were free of cardiovascular disease and cancer at base line. We assessed the consumption of beer, red wine, white wine, and liquor individually every four years using validated food-frequency questionnaires. We documented cases of nonfatal myocardial infarction and fatal coronary heart disease from 1986 to 1998.
During 12 years of follow-up, there were 1418 cases of myocardial infarction. As compared with men who consumed alcohol less than once per week, men who consumed alcohol three to four or five to seven days per week had decreased risks of myocardial infarction (multivariate relative risk, 0.68 [95 percent confidence interval, 0.55 to 0.84] and 0.63 [95 percent confidence interval, 0.54 to 0.74], respectively). The risk was similar among men who consumed less than 10 g of alcohol per drinking day and those who consumed 30 g or more. No single type of beverage conferred additional benefit, nor did consumption with meals. A 12.5-g increase in daily alcohol consumption over a four-year follow-up period was associated with a relative risk of myocardial infarction of 0.78 (95 percent confidence interval, 0.62 to 0.99).
Among men, consumption of alcohol at least three to four days per week was inversely associated with the risk of myocardial infarction. Neither the type of beverage nor the proportion consumed with meals substantially altered this association. Men who increased their alcohol consumption by a moderate amount during follow-up had a decreased risk of myocardial infarction.
Cocoa powder is rich in polyphenols such as catechins and procyanidins and has been shown in various models to inhibit LDL oxidation and atherogenesis.
We examined whether long-term intake of cocoa powder alters plasma lipid profiles in normocholesterolemic and mildly hypercholesterolemic human subjects.
Twenty-five subjects were randomly assigned to ingest either 12 g sugar/d (control group) or 26 g cocoa powder and 12 g sugar/d (cocoa group) for 12 wk. Blood samples were collected before the study and 12 wk after intake of the test drinks. Plasma lipids, LDL oxidative susceptibility, and urinary oxidative stress markers were measured.
At 12 wk, we measured a 9% prolongation from baseline levels in the lag time of LDL oxidation in the cocoa group. This prolongation in the cocoa group was significantly greater than the reduction measured in the control group (-13%). A significantly greater increase in plasma HDL cholesterol (24%) was observed in the cocoa group than in the control group (5%). A negative correlation was observed between plasma concentrations of HDL cholesterol and oxidized LDL. At 12 wk, there was a 24% reduction in dityrosine from baseline concentrations in the cocoa group. This reduction in the cocoa group was significantly greater than the reduction in the control group (-1%).
It is possible that increases in HDL-cholesterol concentrations may contribute to the suppression of LDL oxidation and that polyphenolic substances derived from cocoa powder may contribute to an elevation in HDL cholesterol.
Much has been written about the favourable impact on the body of moderate consumption of red wine. Critical assessment of the literature, however, indicates that beer appears to be just as beneficial in countering diseases such as coronary heart disease. Additionally beer can make a substantial contribution to the diet in respect of certain B vitamins, minerals, antioxidants and perhaps fiber.
It is an established fact that moderate consumption of alcoholic beverages leads to some positive biochemical changes in blood that are widely regarded as indicators of improved prevention of atherosclerosis. However, at present, there are different opinions regarding the biologically active compounds of alcoholic beverages that bring about these changes. This experiment was conducted on 60 male Wistar rats, which were divided into five groups, each of which contained 12 rats: four experimental groups (EG1, EG2, EG3, EG4) and one control group (CG). During 4 weeks, all groups of rats were fed basal diet (BD) supplemented with dry red wine (EG1), beer (EG2), lyophilized dry red wine (EG3), or lyophilized beer (EG4). The rats of the CG were fed BD only. The rats of EG1 and EG2 were fed BD supplemented daily with 2.0 mL of wine and 6.0 mL of beer, respectively. The rats of EG3 and EG4 were fed BD supplemented daily with lyophilized wine and lyophilized beer at a concentration corresponding to an intake of 2.0 mL of original wine and 6.0 mL of original beer, respectively. Before and after completion of the trial, a wide range of laboratory tests including lipids and lipid peroxides were performed. The results of this investigation reveal that both original and lyophilized wine and beer exercise statistically significant beneficial lipidemic and antioxidant effects by reducing total cholesterol (TC), low density lipoprotein cholesterol, triglycerides, and lipid peroxides (P < 0.05 for all) and by elevating the high density lipoprotein cholesterol:TC ratio. There were no statistically significant differences in the results between groups fed BD supplemented with original wine and beer versus groups fed BD supplemented with lyophilized wine and beer. Therefore, it can be concluded that the biologically active compound of these beverages is their dry matter containing inter alia polyphenols in relatively high concentrations.
The importance of the antioxidants contained in foods is well recognized both for preserving the foods themselves and for supplying essential antioxidants in vivo. Among these, the melanoidins formed during food processing and storage represent a significant part of our diet, with an average intake of several grams per day. Melanoidins exhibit antioxidant properties in vitro through their protective effect against reactive oxygen species. Here we investigated the protective effect of the model glucoseglycine melanoidins on oxidative stress induced by adriamycin in hepatocytes isolated from rats. The study was performed by examining cell toxicity (lactate dehydrogenase) release in the medium, lipoperoxidation, protein oxidation, GSH and ATP levels. The addition of 50 µg glucoseglycine melanoidins to the hepatocytes treated with 25 and 75 µM of adriamycin decreased the cell oxidative damage. The cell toxicity, lipoperoxidation and the protein oxidation decreased significantly in the presence of melanoidins. The effect of melanoidins on the intracellular antioxidant GSH when co-incubated the adriamycinhepatocytes with melanoidins resulted in a recovery of GSH levels. Furthermore, from the study of ATP levels we found that the damage to the mitochondria induced by adriamycin is decreased in the presence of melanoidins. According to these results, we suggest that melanoidins are capable of preventing cell oxidation. Based on these mechanisms, the ingestion of melanoidins present in food could be play a role important in the prevention of oxidative damage and prevention the diseases related to free radicals. Copyright © 2004 Society of Chemical Industry
A major shift has occurred in the understanding of the pathogenesis of atherosclerosis, myocardial dysfunction, and other
important cardiovascular diseases. Traditional thinking conceived of atherosclerosis as a bland lipid storage disease. However,
the current thinking regarding this and other cardiovascular disorders recognizes an important role for biological processes
such as inflammation and its inextricably linked companion, oxidative stress, in their pathogenesis. This emerging story of
inflammation as a unifying hypothesis for the pathogenesis of many cardiovascular diseases has swept through contemporary
cardiology and now stands on the threshold of clinical fruition by the application of biomarkers. Currently converging clinical
and experimental evidence has pointed to specific participants in atherothrombosis as potential novel biomarkers. Although
currently there is a lack of sufficient evidence to support wide-scale changes in clinical practice based on the application
of inflammatory biomarkers, the next several years should witness critical tests of the inflammatory hypothesis in the clinic
that may prove useful in modifying the management of both individuals without manifest cardiovascular disease and those with
established cardiovascular disorders. This rapid adoption of the concept of inflammation by practitioners furnishes an example
of how fundamental laboratory research may change clinical practice and improve patient outcomes when translated to practice.
Key WordsAtherothrombosis-atherogenesis-inflammation-biomarkers
The amount of glutathione present in hepatic protein mixed disulfides was determined to be 20–30 nmole/g liver. This was established using two specific enzymatic methods: (a) the coupled assay with DTNB and glutathione (GSSG) reductase and (b) a newly developed test using GSH transferase and 1-chloro-2,4-dinitrobenzene for the estimation of GSH released from proteins after borohydride treatment; further, these results were confirmed by HPLC analysis. Thus, authentic glutathione makes up only 2–6% of the value for total protein mixed disulfides. The latter were determined with the generally employed o-phthalaldehyde assay, which is not necessarily specific for GSH. The amount of glutathione mixed disulfides depends linearly on the content of glutathione disulfide in the liver cell in the range studied. By increasing the GSSG levels from 20 to about 60 nmole/g liver with paraquat, nitrofurantoin or t-butyl hydroperoxide, glutathione protein mixed disulfides are increased by a similar amount.
There is currently considerable interest in the study of cytoprotective effects of natural antioxidants against oxidative stress. However, the cellular response to oxidative stress of the antioxidants may be compromised under conditions of dietary restriction. Therefore, the objective of the present study was to investigate the ability of the (−)-epicatechin, a polyphenol with powerful antioxidant properties in vitro, to attenuate oxidative stress-induced cell damage and to understand the mechanism of its protective action in hepatocytes from overnight fasted rats. Oxidative stress in isolated hepatocytes was induced using tert-butylhydroperoxide and the cellular responses in the form of cell membrane damage, lipid peroxidation and levels of endogenous antioxidants assessed. The results provide evidence that in fasted rat hepatocytes, subjected to oxidative stress, epicatechin inhibits cell membrane damage. In addition, lipid peroxidation and superoxide dismutase and catalase activities return to their control condition. The levels of glutathione peroxidase and glutathione, however, were not significantly different from those without treatment with epicatechin, suggesting that the epicatechin influence on these intracellular antioxidants is not the mechanism of protection.
Atherosclerosis is no longer considered a disorder of lipid accumulation, but a disease process characterized by the dynamic interaction between endothelial dysfunction, subendothelial inflammation and the 'wound healing response' of the vascular smooth muscle cells. Prospective epidemiological studies have unequivocally demonstrated increased vascular risk in individuals with elevated levels of (i) cytokines such as interleukin-6 and tumour necrosis factor-alpha, (ii) cell adhesion molecules such as intercellular adhesion molecule-1 and P-selectin, and (iii) acute-phase proteins such as C-reactive protein, fibrinogen and serum amyloid A. Furthermore, evidence from clinical trials have demonstrated that risk reduction achieved with anti-inflammatory agents such as statins is significantly greater in patients with evidence of inflammation. A number of risk factors for atherogenesis, including infectious agents, have been shown to exert their influence via inflammatory mechanisms. However, despite compelling experimental evidence, clinical studies looking at the role of infection in atherogenesis have lacked consistency. The clinical product of this dynamic process is variable and unpredictable between individuals, even those with apparently similar risk profiles.
The traditional view of atherosclerosis as a lipid storage disease crumbles in the face of extensive and growing evidence that inflammation participates centrally in all stages of this disease, from the initial lesion to the end-stage thrombotic complications. Investigators now appreciate that narrowing arteries do not necessarily presage myocardial infarction and that simply treating narrowed blood vessels does not prolong life. Although invasive approaches such as angioplasty and coronary artery bypass will remain necessary in some cases, we now understand that at least some of the cardiovascular benefits attributable to medical treatment and lifestyle modification (diet and physical activity) may result from reductions in inflammatory processes.
Oxidative stress has been linked to such degenerative diseases as atherosclerosis, and it has been suggested that increased dietary intake of antioxidants may reduce its progression.
To determine the effect of mandarin juice consumption on biomarkers related to oxidative stress in hypercholesterolemic children.
The diet of 48 children with plasma cholesterol >200 mg/dL and low-density lipoprotein cholesterol >130 mg/dL was supplemented for 28 days with 500 mL/day of pure (100%) mandarin juice (Citrus clementina Hort. ex Tan.). The composition of the mandarin juice was analyzed, and its antioxidant antiradical activity was evaluated in vitro. Malondialdehyde, carbonyl groups, vitamins E and C, erythrocyte-reduced glutathione, and plasma lipids were measured at the onset and at the end of the supplementation period. The paired Student t test was used to compare values before and after supplementation.
Mandarin juice exerted a strong antioxidant effect mainly due to its high hydroxyl activity and, to a lesser extent, to its superoxide scavenger activity. At the end of the study, levels of the plasma biomarkers of oxidative stress were significantly decreased (malondialdehyde -7.4%, carbonyl groups -29.1%, P < 0.01), whereas the plasma antioxidants vitamin E and C (13.5%, P < 0.001 and 68.2%, P < 0.00001, respectively) and intraerythrocyte glutathione level (36.7%, P < 0.00001) were significantly increased. Plasma lipids and antibodies to oxidized low-density lipoproteins remained unchanged.
Regular ingestion of mandarin juice significantly reduces plasma biomarkers of lipid and protein oxidation and enhances the antioxidant status of consumers.
A simultaneous determination of retinol, alpha-tocopherol and beta-carotene in serum by high-performance liquid chromatography is described. Total analysis time is 13 min. A reversed-phase (Ultrasphere ODS, 5 microns) column is used with a mobile phase of acetonitrile-methanol-dichloromethane (70:10:20, v/v/v) and a flow-rate of 1.2 ml/min. Retinol is monitored at 325 nm, alpha-tocopherol at 292 nm and beta-carotene at 450 nm. Serum is deproteinized with ethanol containing the internal standard (alpha-tocopherol acetate), then extracted with hexane. The evaporated organic layer is reconstituted with the mobile phase and injected. The choice of the eluent is discussed, as well as the choice of an internal standard and the need for an antioxidant during the extraction step. Sixteen different eluents are compared in terms of analysis time and selectivity. The linear concentration ranges (retinol 0.016-13.7 microM, alpha-tocopherol 0.18-91.8 microM, beta-carotene 0.05-5.75 microM), within-run coefficients of variation (retinol less than 7%; alpha-tocopherol less than 8%, beta-carotene less than 7%), between-run coefficients of variation (retinol less than 13%, alpha-tocopherol less than 9%, beta-carotene less than 8%) and recoveries (retinol greater than 95%, alpha-tocopherol greater than 91%, beta-carotene greater than 80%) are suitable for clinical investigations. Serum reference values were found to be 2.47 +/- 0.61 microM (retinol), 30.5 +/- 6.8 microM (alpha-tocopherol) and 0.91 +/- 0.55 microM (beta-carotene). A significant difference (p less than 0.001) between males and females was found for retinol.
Publisher Summary This chapter discusses methods to determine carbonyl content in oxidatively modified proteins. The methods described are (1) reduction of the carbonyl group to an alcohol with tritiated borohydride; (2) reaction of the carbonyl group with 2,4-dinitrophenylhydrazine to form the 2,4-dinitrophenylhydrazone; (3) reaction of the carbonyl with fluorescein thiosemicarbazide to form the thiosemicarbazone; and (4) reaction of the carbonyl group with fluorescein amine to form a Schiff base followed by reduction to the secondary amine with cyanoborohydride. Van Poelje and Snell have also quantitated protein-bound pyruvoyl groups through formation of a Schiff base with p-aminobenzoic acid followed by reduction with cyanoborohydride. Although a systematic investigation has not appeared, this method should also be useful in detecting other protein-bound carbonyl groups. Carbonyl content of proteins is expressed as moles carbonyl/mole subunit for purified proteins of known molecular weight. For extracts, the results may be given as nanomoles carbonyl/milligram protein. For a protein having a molecular weight of 50,000, a carbonyl content of 1 mol carbonyl/mol protein corresponds to 20 nmol carbonyl/mg proteins.
The evolution of atheromatous lesions is characterized by its slowness, over on several years, for a long time wholly silent, and by the menace of complications which happened brutally, generally threatening lately the functional and vital prognosis. These complications are: reduction of arterial lumen with its hemodynamic consequences, thromboses, embolisms, and more rarely arterial aneurysms. Atherosclerotic lesions have been known for a long time and well described from the macroscopic and histologic points of view. Likewise, the chemical composition of the arterial components at the different steps of the disease is now known. On the contrary many mysteries still remain concerning the pathogenesis of atherosclerosis, and more and more we tend to think that the causes of the disease are numerous and that they start a number of common mechanisms which begin to be best known.
Plasma malondialdehyde-like material (MDA-LM) was evaluated in 138 normal subjects and in a group of 57 stroke patients using a modification of the method of Smith et al. (1976). The basal level of MDA-LM in the control group was 35 mumol/l with a range of 22-50 mumol/l. Values above 50 mumol/l were found in 80% of the patients suffering from subarachnoid haemorrhage, in 68% of those with cerebral thrombosis, and in 17% with transient ischaemic attacks. None of the patients with cerebral embolism, intracerebral haematoma, or lacunar infarct had values above 50 mumol/l. Significant statistical differences were found between the control group and all the patients except those with lacunar infarcts.
The clinical events resulting from atherosclerosis are directly related to the oxidation of lipids in LDLs that become trapped in the extracellular matrix of the subendothelial space. These oxidized lipids activate an NF kappa B-like transcription factor and induce the expression of genes containing NF kappa B binding sites. The protein products of these genes initiate an inflammatory response that initially leads to the development of the fatty streak. The progression of the lesion is associated with the activation of genes that induce arterial calcification, which changes the mechanical characteristics of the artery wall and predisposes to plaque rupture at sites of monocytic infiltration. Plaque rupture exposes the flowing blood to tissue factor in the lesion, and this induces thrombosis, which is the proximate cause of the clinical event. There appear to be potent genetically determined systems for preventing lipid oxidation, inactivating biologically important oxidized lipids, and/or modulating the inflammatory response to oxidized lipids that may explain the differing susceptibility of individuals and populations to the development of atherosclerosis. Enzymes associated with HDL may play an important role in protecting against lipid oxidation in the artery wall and may account in part for the inverse relation between HDL and risk for atherosclerotic clinical events.
4-Hydroxy-2,3-trans-nonenal, a lipid peroxidation product, inhibits glutathione peroxidase in a concentration-dependent manner. The concentration providing 50% inhibition is 0.12 mM. This inhibition can be almost completely (89%) prevented by 1 mM glutathione added to the incubation mixture 30 min before 4-hydroxy-2,3-trans-nonenal or 2,3-trans-nonenal, but not by other thiol-containing antioxidants such as 0.5 mM dithiothreitol or beta-mercaptoethanol. Again the addition of 1 mM glutathione, and not of 0.5 mM dithiothreitol or beta-mercaptoethanol, to the enzyme 30 min after incubation with 4-hydroxy-2,3-trans-nonenal restores activity to the same extent as does the preincubation with GSH. In view of the known reactivity of 4-hydroxy-2,3-trans-nonenal with lysine residues and the reversibility of the inhibition, the involvement of a lysine residue in GSH binding to glutathione peroxidase is proposed. The potential relevance of the inhibition of glutathione peroxidase by 4-hydroxy-nonenal to oxidative tissue damage is discussed with particular emphasis on neurological disorders.
The positive association of a moderate intake of alcoholic beverages with a low risk for cardiovascular disease, in addition to ethanol itself, may be linked to their polyphenol content. This article describes the effect of acute ingestion of beer, dealcoholized beer, and ethanol (4.5% v/v) on the total plasma antioxidant status of subjects, and the change in the high performance liquid chromatography profile of some selected phenolic acids (caffeic, sinapic, syringic, and vanillic acids) in 14 healthy humans. Plasma was collected at various times: before (T0), 1 hour after (T1), and 2 hours after (T2) drinking. The study is part of a larger research planned to identify both the impact of brewing on minor components potentially present in beer and their metabolic fate in humans. Beer was able to induce a significant (P < 0.05) increase in plasma antioxidant capacity at T1 (mean +/- SD: T0 1,353 +/- 320 microM; T1 1,578 +/- 282 microM), returning close to basal values at T2. All phenolic acids measured in plasma tended to increase after beer intake (20% at T1, 40% at T2). Syringic and sinapic acid reached statistical significance (P < 0.05 by one-way analysis of variance-Fisher's test) at T1 and T2, respectively. Plasma metabolic parameters (glucose, total cholesterol, triglycerides, and uric acid) and plasma antioxidants (alpha-tocopherol and glutathione) remained unchanged. Ethanol removal impaired the absorption of phenolic acids, which did not change over the time of the experiment, accounting for the low (and not statistically significant) increase in plasma antioxidant capacity after dealcoholized beer drinking. Ethanol alone did not affect plasma antioxidant capacity or any of the antioxidant and metabolic parameters measured.
Moderate alcohol consumption (1-2 drinks/d) may decrease cardiovascular disease risk in postmenopausal women by improving lipid profiles.
We measured the effect of moderate alcohol consumption on lipids and lipoproteins in postmenopausal women.
Postmenopausal women (n = 51) consumed 0 (control), 15 (1 drink), and 30 (2 drinks) g alcohol (ethanol)/d for 8 wk each as part of a controlled diet in a randomized crossover design. The control diet provided approximately 15%, 53%, and 32% of energy from protein, carbohydrate, and fat, respectively. The energy provided from alcohol in the 15- and 30-g alcohol diets was replaced with energy from carbohydrate.
Compared with concentrations after the control diet, plasma LDL cholesterol decreased from 3.45 to 3.34 mmol/L (P = 0.04) and triacylglycerol from 1.43 to 1.34 mmol/L (P = 0.05) after 15 g alcohol/d. There were no additional significant decreases in either lipid after an increase in alcohol intake from 15 to 30 g/d. Compared with concentrations after the control diet, plasma HDL cholesterol increased nonsignificantly from 1.40 to 1.43 mmol/L after 15 g alcohol/d but increased to 1.48 mmol/L after 30 g alcohol/d (P = 0.02). Apolipoprotein A-I increased significantly and apolipoprotein B decreased significantly after 30 g alcohol/d relative to the concentration after the control diet.
Consumption of 15-30 g alcohol/d by postmenopausal women apparently decreases cardiovascular disease risk by improving lipid profiles. Plasma LDL-cholesterol and triacylglycerol concentrations improve after 15 g alcohol/d; plasma HDL cholesterol improves only after 30 g alcohol/d.
Recent interest in food phenolics has increased greatly, because of their antioxidant and free radical scavenging abilities. Popular beverages in the world include tea, coffee, cocoa, beer, wine and fruit/vegetable juices. All of these beverages contain phenolic compounds. In present study total polyphenol content and in vitro antioxidant properties were investigated in 16 red wines, 5 white wines, 5 lager beers, 3 dark beers, 17 fruit juices and 5 vegetable juices. High polyphenol content was measured in red wines (1720 +/- 546 mg x L(-1)) and in some fruit juices such as elderberry and prunes (5,680 and 1,807 mg x L(-1), respectively). The concentration of polyphenols was between 159 and 5,680 mg x L(-1) in fruit juices and between 255 and 696 mg x L(-1) in vegetable ones, while low level of phenolics was observed in dark and lager beers and white wines (473, 376 and 392 mg x L(-1), respectively). All samples exhibited significant antioxidant properties such as hydrogen-donating ability, reducing power, chelating ability and total antioxidant status (TAS) value. These antioxidant properties strongly correlated with the total polyphenol content of the beverages.
The free phenols have been measured in 15 lagers, 6 porters and ales, and 11 light and nonalcoholic beers. Phenols were measured colorimetrically using an oxidation-reduction reaction with Folin-Ciocalteu reagent and catechin as the standard. The order of phenol concentration was ales > lagers > low calorie > nonalcoholic. The quality of antioxidants of the major phenols in beers and the quality of beer antioxidants were measured by (1) dose-response inhibition of lower density lipoprotein oxidation and (2) concentration of phenols in the beers at which 50% of the peroxide was destroyed in a luminescent assay for antioxidant activity. The beers' lipoprotein antioxidant quality was clearly superior to that of vitamin antioxidants and to that of the phenol ingredients, suggesting synergism among the antioxidants in the mixture. The average per capita consumption of beer in the United States in 2000 was 225 mL/day, equivalent to 42 mg/day of catechin equivalents. Beer provides more antioxidants per day than wine in the U.S. diet. A dark beer and a lager beer were given at two concentrations to cholesterol-fed hamsters, an animal model of atherosclerosis. At the high dose ((1)/(2)-diluted beer) both lager and dark beer significantly inhibited atherosclerosis compared to a control of 2% alcohol. At the high dose, lager significantly decreased cholesterol and triglycerides, and both beers acted as in vivo antioxidants by decreasing the oxidizability of lower density lipoproteins. At the low dose ((1)/(10)-diluted beer) only the lager beer significantly decreased atherosclerosis compared to the 0.4% alcohol control. The polyphenols in the beers appear to be responsible for the benefits of beer in this model. Lager beer inhibited atherosclerosis at a human equivalent dose in this hamster model of atherosclerosis.
MODERATE BEER CONSUMPTION (MBC) IS CARDIOPROTECTIVE: it positively influences plasma lipid levels and plasma antioxidant activity in beer-consuming individuals. The connection between MBC and blood coagulation is not clearly defined. Forty-two volunteers were equally divided into experimental (EG) and control (CG) groups following coronary bypass surgery. For 30 consecutive days, only patients of the EG consumed 330 mL of beer per day (about 20 g of alcohol). A comprehensive clinical investigation of 42 patients was done. Blood samples were collected before and after the investigation for a wide range of laboratory tests. The plasma fibrinogen was denatured with 8 M urea and intrinsic fluorescence (IF), hydrophobicity and differential scanning calorimetry (DSC) were used to reveal possible qualitative changes. After 30 days of moderate beer consumption, positive changes in the plasma lipid levels, plasma anticoagulant and plasma antioxidant activities were registered in patients of the EG group. In 17 out of 21 patients of the same group, differences in plasma circulating fibrinogen's (PCF), secondary and tertiary structures were found. The stability of fibrinogen, expressed in thermodynamic parameters, has shown that the loosening of the structure takes place under ethanol and urea denaturation. Also fluorescence stability of PCF was decreased. No changes in the lipid levels, anticoagulant and antioxidant activity or changes in PCF were detected in patients of CG. In conclusion, for the first time after a short term of moderate beer consumption some qualitative changes in the plasma circulating fibrinogen were detected: differences in the emission peak response, fluorescence intensity and all thermodynamic data. Together, with the decrease in the PCF concentration it may lead to an elevation of the blood anticoagulant activity.
The beneficial effect of moderate alcohol consumption in lowering the risk of cardiovascular disease has been shown in several epidemiologic studies. Such studies have also shown, however, that the protective effect of alcoholic beverages like wine and beer is not only due to the ethanol content but also to the presence of nonalcoholic constituents. The positive effect of alcoholic beverages has been attributed to changes in lipoprotein metabolism, but there is substantial evidence that effects on hemostasis play an important role. Whether the effects of alcoholic beverages on hemostasis are due exclusively to ethanol or are due, in part, to nonalcoholic components, is still under debate.
We have examined the hemostatic effects of 3 liters of beer, dealcoholized beer, and ethanol/water (v/v 4%), consumed over a period of 3 hr, in 12 young healthy volunteers. Platelet parameters CD62, PAC-1, and monocyte platelet aggregates were analyzed using flow cytometric measurements. The activity of factor VII was determined with a prothrombin time (PT) assay and plasminogen activator inhibitor activity using a chromogenic substrate. Thrombin generation was determined according to the method of Hemker.
All three fluids administered, dealcoholized beer, beer, and ethanol, reduced the expression of activated fibrinogen receptor, the platelet activation marker CD62, and the formation of monocyte-platelet-aggregate. In addition, dealcoholized beer also showed significant inhibitory effects on thrombin generation, whereas beer and ethanol showed procoagulatory effects.
This study has shown that the acute consumption of dealcoholized beer inhibits thrombogenic activity in young adults. This action could have a beneficial effect on the development of coronary artery disease. Thus, the consumption of dealcoholized beer could provide cardiovascular benefit without the negative effects of alcohol.
Anti-inflammatory effects of moderate alcohol consumption have been proposed to explain why moderate alcohol intake lowers coronary heart disease risk. We investigated the relationship between overall alcohol, beer or wine consumption and markers of systemic inflammation in three different geographical areas in Europe.
Cross-sectional samples, each representative of the general population from Germany, Scotland, and France (MONICA Augsburg 1994/95, 2275 men and 2186 women, 25-74 years; Glasgow MONICA 1994/95, 561/616, 25-74 years, and MONICA Lille 1994/95, 581/574, 35-64 years) were studied. Alcohol intake was assessed by standardized interview. Adjusted means of C-reactive protein (CRP), fibrinogen, white blood cell (WBC) count, plasma viscosity (PV), and albumin were calculated among categories of alcohol intake, and separately for beer or wine consumption, by multiple linear regression. Self-reported moderate daily alcohol intake up to 40 g was associated with lower concentrations of CRP, fibrinogen, PV and WBC count, compared to non-drinking and heavy drinking, even after adjustment for various potential confounders.
Moderate consumption of either wine or beer is associated with lower levels of systemic inflammatory markers in three different European areas, suggesting that ethanol itself might be largely responsible for the potential anti-inflammatory effects of these beverages.
Beers are a source of dietary flavonoids; however, there exist differences in composition, alcohol concentration, and beneficial activities. To characterize these differences, three kinds of lager beer of habitual consumption in Spain, dark, blond, and alcohol-free, were assayed for total phenolic content, antioxidant activity, superoxide and hydroxyl radical scavenging activities, and in vitro inhibitory effect on DNA oxidative damage. Furthermore, their melanoidin content and correlation with antioxidant activity were evaluated. Dark beer contained the highest total phenolic (489 +/- 52 mg/L) and melanoidin (1.49 +/- 0.02 g/L) contents with a 2-fold difference observed when compared to the alcohol-free beer. For the three kinds of beer, the antioxidant activity measured as N,N-dimethyl-p-phenylenediamine dihydrochloride concentration was strongly correlated with the total polyphenol content (R(2) = 0.91102, p < 0.005) and with the melanoidin content (R(2) = 0.7999, p < 0.05). The results support a positive effect of beers on the protection of DNA oxidative damage, by decreasing the deoxyribose degradation, DNA scission (measured by electrophoresis), and inhibition of 8-hydroxydeoxyguanosine (8-OH-dG) formation. Furthermore, a correlation between the total melanoidin content (R(2) = 0.7309, p < 0.01) and inhibition of 8-OH-dG was observed.
A high-performance liquid chromatography (HPLC) method to determine malondialdehyde (MDA) as the 2,4-dinitrophenylhydrazine (DNPH) derivative was applied to biological samples (serum and liver homogenates). Since MDA is considered a presumptive biomarker for lipid peroxidation in live organisms, a model for nutritionally induced oxidative stress (hypercholesterolemic rats) was studied in comparison with normocholesterolemic animals. The effect of diet supplementation with fruits rich in antioxidant polyphenols was assessed. The proposed method showed to be precise and reproducible, as well as sensitive enough to reflect differences in the oxidative status in vivo. A significant decrease of serum and liver MDA concentrations in animals fed diets containing 0.3% of polyphenols from strawberry, cocoa or plum was observed in the normocholesterolemic groups. This reduction was especially noteworthy in the hypercholesterolemic animals, with increased MDA levels indicating enhanced lipid peroxidation in the controls, yet with values parallel to the normocholesterolemic groups in animals fed the polyphenol-rich diets. These results point out the beneficial effects of phenolic antioxidants from fruits in preventing oxidative damage in vivo.
In spite of the wide literature describing the biological effects of phenolic compounds, scarce data are available on their absorption from diet. In the present work, we studied the absorption in humans of phenolic acids from beer, a common beverage rich in different phenolic acids with related chemical structures. Beer was analyzed for free and total (free+bound) phenolic acids. Ferulic, caffeic and sinapic acids were present in beer mainly as bound forms, while 4-hydroxyphenylacetic acid and p-coumaric acid were present mainly as free forms. Vanillic acid was present equally in the free and bound forms. Plasma samples were collected before and 30 and 60 min after beer administration and analyzed for free and conjugated phenolic acid content. A significant two- to fourfold increase in plasma levels of phenolic acids was detected with peak concentrations at 30 min after beer ingestion. 4-Hydroxyphenylacetic acid was present in plasma mainly as nonconjugated forms while p-coumaric acid was present equally as nonconjugated and conjugated forms. Ferulic, vanillic and caffeic acids were present in plasma predominantly as conjugated forms, with a slight prevalence of sulfates with respect to glucuronates. Our results indicate that phenolic acids from beer are absorbed from the gastrointestinal tract and are present in blood after being largely metabolized to the form of glucuronide and sulfate conjugates. The extent of conjugation is related to the chemical structure of phenolic acids: the monohydroxy derivatives showing the lowest conjugation degree and the dihydroxy derivatives showing the highest one.
Several naturally occurring constituents have received considerable attention because of their potential antioxidant activity. Consuming a diet rich in natural antioxidants has been associated with prevention from and/or treatment of atherosclerosis. Bioactive components of food, which are of special interest, include the Vitamins E and C, polyphenols, carotenoids-mainly lycopene and beta-carotene, and coenzyme Q10, featured by antioxidant properties. Antioxidant therapy is supposed to be effective in the early stages of atherosclerosis by preventing LDL oxidation and the oxidative lesion of endothelium. This review focuses on the effect of dietary antioxidants pertained to LDL oxidation and to the vascular endothelial dysfunction. Now that the human genome has been completely sequenced, genetic factors involved in oxidation may open new horizons to identify persons at risk for cardiovascular disease, allowing effective dietary intervention strategies to recover normal homeostasis and to prevent diet-related implications. On this basis, current studies on the action of selected antioxidant nutraceuticals on the activity of transcription factors, such as final targets in the signal transduction cascade and gene regulation, may emerge into new treatment concepts.
Defatted milled grape seed (DMGS) is a wine by-product obtained from the oil extraction of the grape seed that contains different types of phenolic compounds. The present study was designed to evaluate the possible protective effect of DMGS on toxicity induced by adriamycin (ADR) in isolated rat hepatocytes. The study was carried out by examining the results of lactate dehydrogenase (LDH) release to estimate cytotoxicity; the thiobarbituric acid reactant substances (TBARS) and carbonyl group levels were measured as biomarkers of oxidative stress and ATP and GSH levels as estimation of intracellular effect. The results showed that DMGS extract protects the cellular membrane from oxidative damage and consequently prevents protein and lipid oxidation. The levels of ATP and GSH changes for the ADR toxicity were restored to control value in the presence of DMGS extract. The experimental results suggest that this wine by-product may be used to decrease oxidative stress.
Increased fruit and vegetable consumption is associated with a decreased incidence of cardiovascular diseases, cancer, and other chronic diseases. The beneficial health effects of fruits and vegetables have been attributed, in part, to antioxidant flavonoids present in these foods. Large, transient increases in the total antioxidant capacity of plasma have often been observed after the consumption of flavonoid-rich foods by humans. These observations led to the hypothesis that dietary flavonoids play a significant role as antioxidants in vivo, thereby reducing chronic disease risk. This notion, however, has been challenged recently by studies on the bioavailability of flavonoids, which indicate that they reach only very low concentrations in human plasma after the consumption of flavonoid-rich foods. In addition, most flavonoids are extensively metabolized in vivo, which can affect their antioxidant capacity. Furthermore, fruits and vegetables contain many macro- and micronutrients, in addition to flavonoids, that may directly or through their metabolism affect the total antioxidant capacity of plasma. In this article, we critically review the published research in this field with the goal to assess the contribution of dietary flavonoids to the total antioxidant capacity of plasma in humans. We conclude that the large increase in plasma total antioxidant capacity observed after the consumption of flavonoid-rich foods is not caused by the flavonoids themselves, but is likely the consequence of increased uric acid levels.
Extracted total phenols, flavanols and flavonoids were measured in beer samples and their quality as antioxidants was measured by two modified antioxidant methods: the 2,2'-azinobis (3-ethylbenzothiazoline-6-sulfonate) radical cation (ABTS * +) and the beta-carotene-linoleate model system (beta-carotene). It was found that the antioxidant potential of beer was well correlated with flavanols and flavonoids and was slightly lower with total polyphenols (R2 values from 0.8203 to 0.9393). Forty-two male non drinkers, hypercholesterolaemic volunteers ages 43-71 after coronary bypass surgery, were randomly divided into experimental (EG) and control (CG) groups, each of 21 participants. The antiatherosclerotic diet of the EG group was supplemented for 30 consecutive days with 330 ml beer per day. Could short-term beer consumption affect not only the risk factors of coronary atherosclerosis, but also the markers of this process: plasma albumin and its antioxidant activity? For this goal, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, plasma albumin and fibrinogen, and the antioxidant activity were determined. After the trial a significant improvement in the plasma lipid levels, and an increase in the plasma antioxidant and anticoagulant activities in patients of the EG group was registered. A parallel increase in the plasma albumin concentration and its antioxidant activity was observed. In conclusion, short-term beer consumption on the basis of the bioactivity of the beverage positively affects plasma lipid levels, plasma antioxidant and anticoagulant activities. The increase in the plasma albumin concentration and its antioxidant activity could be the markers of atherosclerosis status.
To analyse the association of moderate beer consumption on the blood lipid profile in healthy Spanish adults.
The study had an intervention longitudinal design in which each subject established their own control with a previous wash-out phase. After a 30-day alcohol abstinence period, 57 healthy volunteers were submitted to a daily moderate intake of beer for 30 days. Serum total cholesterol, HDL-cholesterol, triacylglycerols, GOT, GPT, GGT and glucose values, as well as blood erythrocytes, haemoglobin, haematocrit and MCV levels, together with anthropometric parameters were determined at the beginning of the study (baseline levels) (a), after 1 month of alcoholic abstinence (b) and after 1 month of moderate beer consumption (c). Dietary intake was assessed twice by a 7-day dietary record. HDL-cholesterol, erythrocytes, haematocrit and MCV levels increased significantly (p<0.05) after moderate beer consumption in women. In men, a decrease in HDL-cholesterol levels was observed after alcohol abstention. Haematocrit and MCV counts also increased significantly (p<0.05) in men after moderate beer consumption. There were no dietary changes during the study.
In healthy Spanish adults, the effects of moderate beer consumption during 1 month were associated with favourable changes on the blood lipid profile.
Inflammation plays an important role in the initiation and progression of atherosclerosis but many of its underlying mechanisms remain to be explored. Atherosclerotic plaques which are more prone to destabilisation and rupture, leading to clinical events, are characterised by increased infiltration of leukocytes and other inflammatory mediators, compared with stable fibrotic plaques. T cell mediated responses, through expression of cytokines and chemokines, play an important role in the inflammatory process; and more recently potentially anti-inflammatory markers have also been identified. Current management involves both mechanical restoration of blood flow and pharmacotherapy aimed in part at suppressing the underlying inflammatory mechanisms. The aims of this review are to outline the pro- and anti-inflammatory processes in atherosclerosis, as well as their clinical implications.
Cardiovascular disease is the leading cause of death and morbidity among postmenopausal women, and oestrogen deficiency may be an important factor in its development. The role of oestrogen replacement in preventing cardiovascular disease is controversial. The aim of this descriptive review is to analyse the available data and to recommend evidence-based practice guidelines pertaining to hormone therapy in the context of cardiovascular and cerebrovascular health.
Relevant clinical trials were identified by computerised literature search. The collated data were presented to fellow gynaecologists for review, analysis of results and discussion in a series of meetings dedicated to finding the best evidence in menopause management. The evidence was used to formulate clinical practice guidelines for the management of women with significant cardiovascular risk factors.
Evidence from animal studies and observational trials supported a cardio-protective effect of postmenopausal hormone therapy. More recent randomised clinical trial data have shown no significant reduction of coronary heart disease, and have confirmed a higher incidence of stroke and venous thromboembolism.
The evidence is widely divergent regarding postmenopausal hormone therapy and cardiovascular risk. More consistent data are available reporting an increased risk in the incidence of venous thromboembolism and stroke. It is important to be clear about the indications of hormone use and to utilise alternative modalities to promote cardiovascular health in the postmenopausal population.
Beer increases plasma antioxidant capacity in humans Overall alcohol intake, beer, wine, and systemic markers of inflammation in Western Europe: results from three MONICA samples
- A Ghiselli
- F Natella
- A Guidi
- L Montanari
- P Fantozzi
- C Scaccini
- A Imhof
- M Woodward
- A Doering
- N Helbecque
- H Loewel
- P Amouyel
Ghiselli A, Natella F, Guidi A, Montanari L, Fantozzi P, Scaccini C. Beer increases plasma antioxidant capacity in humans. J Nutr Biochem 2000;11:76 – 80. [7] Imhof A, Woodward M, Doering A, Helbecque N, Loewel H, Amouyel P, et al. Overall alcohol intake, beer, wine, and systemic markers of inflammation in Western Europe: results from three MONICA samples (Augsburg, Glasgow, Lille). Eur Heart J 2004;25: 2092–100.
Determination of malondialdehyde (MDA) by high-performance liquid chromatography in serum and liver as a biomarker for oxidative stress
- Mateos