No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
Alcohol Dosing and the Heart: Updating Clinical Evidence
Abstract
The consequences of heavy or irregular alcohol drinking have long been known. Recently, consistent information has been provided in support of an association between light/moderate alcohol consumption and protection from vascular and all-cause mortality, ischemic stroke, peripheral arterial disease, congestive heart failure, and recurrence of ischemic events. After reviewing the information with respect to major aspects of cardiovascular pathophysiology, to potential confounders and to underlying mechanisms, several concepts emerge. First, the recommended amounts of "safe alcohol drinking" in healthy individuals are up to two standard drinks (~20 g/d) for a man and up to one drink (10 g/d) for a nonpregnant woman. The overall balance for young premenopausal women, but not for older women, would be unfavorable for drinking. The risk of cancer would not outweigh potential benefits of alcohol on heart disease. Second, within the frame of a balanced pattern of dietary energy intake, patients with cardiovascular disease who drink alcohol should not exceed one or two standard drinks per day for women or up to two or three drinks per day for men. Third, the low rates of coronary heart disease among the Mediterranean people may be related to their pattern of drinking wine every day during meals. Regular drinking is associated with better outcomes than occasional (binge)/weekly drinking. Fourth, wine (ethanol with antioxidants) exhibits significantly higher anti-inflammatory effects than gin (ethanol without polyphenols), and thus in general wine should be preferred to liquor or beer.
... Although future research on drinking trajectories and mortality risk within the WHI would help address this issue, data from another longitudinal study of women over the age of 50 found that relatively few (approximately 11%) significantly increased or decreased their drinking levels over a 10-year period (Bobo & Greek, 2011). We also did not differentiate between types of alcoholic beverages consumed (i.e., beer, wine [red vs. other], spirits), which may have obscured protective or harmful effects associated with particular type of alcohol consumed (Di Minno et al., 2011). Additionally, because the data were unavailable, we did not take into account the amount of drinking per occasion. ...
Purpose:
To address research gaps regarding women Veterans’ alcohol consumption and mortality risk as compared to non-Veterans, the current study evaluated whether alcohol consumption amounts differed between women Veterans and non-Veterans, whether Veterans and non-Veterans within alcohol consumption groups differed on all-cause mortality, and whether Veteran status modified the association between alcohol consumption and all-cause mortality.
Design and Methods:
Six alcohol consumption groups were created using baseline data from the Women’s Health Initiative Program (N = 145,521): lifelong abstainers, former drinkers, less than 1 drink/week (infrequent drinkers), 1–7 drinks/week (moderate drinkers), 8–14 drinks/week (moderately heavy drinkers), and 15 or more drinks/week (heavy drinkers). The proportions of Veteran and non-Veteran women within each alcohol consumption category were compared. Mortality rates within each alcohol consumption category were compared by Veteran status. Cox proportional hazard models, including a multiplicative interaction term for Veteran status, were fit to estimate adjusted mortality hazard (rate) ratios for each alcohol consumption category relative to a reference group of either lifelong abstainers or moderate drinkers.
Results:
Women Veterans were less likely to be lifelong abstainers than non-Veterans. Women Veterans who were former or moderate drinkers had higher age-adjusted mortality rates than did non-Veterans within these alcohol consumption categories. In the fully adjusted multivariate models, Veteran status did not modify the association between alcohol consumption category and mortality with either lifelong abstainers or moderate drinkers as referents.
Implications:
The results suggest that healthcare providers may counsel Veteran and non-Veteran women in similar ways regarding safe and less safe levels of alcohol consumption.
... On the other hand, a meta-analysis of eight publications revealed that in patients with cardiovascular disease, light to moderate alcohol consumption (5 to 25 g/day) was significantly associated with a lower incidence of cardiovascular and all-cause mortality (Costanzo et al., 2010a). Causal impact of average volume of alcohol consumption, i.e. dosing effect, on the reported outcomes was explained recently (Di Minno et al., 2011). In addition, methodological issues, drinking patterns, beverage type or gender differences should be considered in the interpretation of the current controversial and somehow odd figure of association between ethanol consumption and risk of cardiovascular disease (Brinton, 2010;da Luz and Coimbra, 2004;Fuchs et al., 2001;Kauhanen et al., 1999;Kloner and Rezkalla, 2007). ...
Chronic ethanol consumption increases the incidence of cardiovascular disease. The mechanisms underlying ethanol-induced susceptibility to cardiovascular disease continue to be defined. This study examines the hypothesis that chronic ethanol consumption plausibly induces vascular wall abnormalities via inflammatory reactions. In addition, it intends to find out whether vitamin E inhibits the abnormalities induced by ethanol in rats' vascular wall. Twenty four male Wistar rats were divided into three groups (n=8): Control ©, ethanol (E), and vitamin E treated ethanol (VETE) group. After 6weeks, the aortic and coronary wall changes, vascular endothelial growth factor (VEGF), alpha-1 glycoprotein and haptoglobin amounts in plasma, C-reactive protein levels(CRP), as well as the amount of aortic IL-6 were evaluated. The results revealed the elevation of polymorphonuclear (PMN) leukocyte in the vascular wall, disorganization of endothelium with ballooning of cells, proliferation of vasa-vasorum with an increase in the IL-6, CRP, as well as a decrease in VEGF and an increase in alpha-1 glycoprotein and haptoglobin in the ethanol group compared to the control group. Significant amelioration of aortic and coronary wall changes, along with the restoration of elevated level of IL6, CRP, and the decreased level of VEGF compared to that of the controls were found in vitamin E-treated animals. These findings strongly support the idea that heavy and chronic ethanol consumption initiates atherosclerosis by inflammatory stress, and that these effects can be alleviated by vitamin E as an anti-inflammatory agent.
... Pre-menopausal women have a lower incidence of CVD, and therefore, the effects of moderate alcohol consumption might be lower (Di Castelnuovo et al., 2006). In addition, teenagers and young adults tend to have unhealthier drinking patterns such as binge drinking (defined as 3-5 drinks within 2 h), which is unquestionably harmful (Di Minno et al., 2011). ...
AimsThe aim of this review was to focus on the knowledge of the cardiovascular benefits of moderate alcohol consumption, as well as to analyze the effects of the different types of alcoholic beverages.Methods
Systematic revision of human clinical studies and meta-analyses related to moderate alcohol consumption and cardiovascular disease (CVD) from 2000 to 2012.ResultsHeavy or binge alcohol consumption unquestionably leads to increased morbidity and mortality. Nevertheless, moderate alcohol consumption, especially alcoholic beverages rich in polyphenols, such as wine and beer, seems to confer cardiovascular protective effects in patients with documented CVD and even in healthy subjects.Conclusions
In conclusion, wine and beer (but especially red wine) seem to confer greater cardiovascular protection than spirits because of their polyphenolic content. However, caution should be taken when making recommendations related to alcohol consumption.
... On the other hand, a meta-analysis of eight publications revealed that in patients with cardiovascular disease, light to moderate alcohol consumption (5 to 25 g/day) was significantly associated with a lower incidence of cardiovascular and all-cause mortality (Costanzo et al., 2010a). Causal impact of average volume of alcohol consumption, i.e. dosing effect, on the reported outcomes was explained recently (Di Minno et al., 2011). In addition, methodological issues, drinking patterns, beverage type or gender differences should be considered in the interpretation of the current controversial and somehow odd figure of association between ethanol consumption and risk of cardiovascular disease (Brinton, 2010;da Luz and Coimbra, 2004;Fuchs et al., 2001;Kauhanen et al., 1999;Kloner and Rezkalla, 2007). ...
Controversy exists on whether alcohol has a direct cardioprotective effect or it provokes atherosclerosis, so the present study sought to assess the effect of chronic consumption of ethanol on the markers of endothelial function, vessel rigidity, and atherosclerosis in the aorta of rat. Male Wistar rats were selected randomly and exposed to ethanol (4.5g⁄kg of 20% w/v solution in saline) once per day for 6weeks. Blood pressure, hemodynamic parameters, foam cell formation, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, endothelial-leukocyte adhesion molecule-1, and high-sensitivity C-reactive protein (CRP) were assessed in ethanol treated rats and compared with either sham or control rats. The results revealed a concurrent significant increase of adhesion molecules, CRP levels, systolic, diastolic, pulse, and dicrotic pressures as well as enhanced formation of foam cell in ethanol-treated rats. These findings implicate that long-term ethanol exposure provokes atherogenic and hemodynamic changes via significant induction of proinflammatory response, augmenting of cell adhesion molecules, stiffness in rat aorta wall and induction of foam cell formation.
Background:
Hypertriglyceridemia affects 15-20% of the adult population and is associated with overweight, metabolic syndrome, and diabetes mellitus. It is often discovered incidentally.
Methods:
This review is based on pertinent publications retrieved by a selective literature search, including current guidelines on hypertriglyceridemia.
Results:
Elevated triglyceride (TG) levels are causally linked to cardiovascular disease; TG levels above 1000 mg/dL (11.4 mmol/L) can induce acute pancreatitis. The individual risk of cardiovascular disease and of pancreatitis must be estimated in order to decide whether, and how, hypertriglyceridemia should be treated. Lifestyle modifications (cessation of alcohol consumption, reduced intake of rapidly metabolized carbohydrates), weight loss, and blood sugar control are the most effective ways to lower TG levels. The need to lower the low-density lipoprotein (LDL) concentration must be determined on the basis of the cardiovascular risk, independently of the success of the lifestyle changes. Few patients need specific drug treatment to lower the TG level. Fibrates can lower TG concentrations, but their efficacy in combination with statins has not been clearly shown in endpoint studies. A daily dose of 2-4 g omega-3 fatty acids can also lower TG levels. To date, only a single large-scale randomized, blinded trial has shown the efficacy of 4 g of eicosapentaenoic acid ethyl ester per day in lowering the risk in high-risk patients (number needed to treat = 21). Patients with the very rare purely genetic types of hypertriglyceridemia (familial chylomicronemia syndrome) should be treated in specialized outpatient clinics.
Conclusion:
Hypertriglyceridemia is causally linked to cardiovascular disease and pancreatitis. Lifestyle modifications play a paramount role in its treatment.
Introduction: the aim of this review was focusing on the knowledge of the cardiovascular benefits of moderate alcohol consumption, as well as analyzing the effects of the different kinds of alcoholic beverages. Discussion: heavy or binge alcohol consumption unquestionably leads to an increased morbidity and mortality. Nevertheless, moderate alcohol consumption, especially alcoholic beverages rich in polyphenols, such as wine and beer, seems to confer cardiovascular protective effects in patients with documented CVD and even in healthy subjects. Conclusions: in conclusion, wine and beer (and especially red wine) seem to confer greater cardiovascular protection than spirituous beverages because of their polyphenolic content. However, caution should be taken when drinking and social recommendations related to alcohol consumption should be followed.
Objective To establish an acute heart failure model induced by alcohol in rabbits. Methods After rabbits were anesthetized and fixed, femoral artery intubation was used for blood pressure (BP) measurement; left ventricle intubation via carotid was used to detect left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP) and ±dp/dt max. Electrocardiogram was recorded through subcutaneous needle electrode. Acute heart failure model was induced by intravenous injection of alcohol (250 mL/L, 1.0 mL/min) at a constant speed. Hearts were harvested after that and analyzed by histological hematoxylin-eosin staining. Results Compared with the normal hemodynamic indexes before model establishment, the SBP, DBP, MBP, LVSP and ±dp/dt max decreased (P<0.05). Electrocardiogram result showed that heart rate decreased (P<0.05), the duration of P wave, P-R interval, QRS and Q-T intervals were prolonged obviously compared to the baselines (P<0.05). Pathological examination demonstrated that the cardiac muscular tissues of the model were damaged, which was consistent with the pathological manifestation of heart failure. Conclusion Alcohol can be used to induce acute heart failure, which provides a considerable model for investigation of mechanism and therapy of acute alcohol intoxication-induced hear failure.
In dieser Dissertation wurde die Bedeutung der TRAFs in der Koronaren Herzerkrankung im Rahmen der prospektiven „TRAFs in Cardiovascular Disease“ (TRAFIC) – Studie untersucht. Es zeigte sich, dass die RNA-Expressionen von TRAF1, -4, -5 und -7 mit der stabilen bzw. instabilen Koronaren Herzerkrankung korrelieren. TRAF2, -3 und -6 dagegen zeigten keine Unterschiede in den RNA-Expressionen in Patienten. Zusätzlich wurde die Eignung der TRAFs als prognostische Faktoren untersucht. Hierbei ergab die statistische Analyse, dass sich die sieben TRAFs weniger als prognostischer Biomarker zu eignen scheinen, wenngleich TRAF2-7 mit dem Auftreten von kardiovaskulären Ereignissen deutlich negativ korrelieren. In einer genetischen Analyse wurden außerdem fünf Single-Nukleotid-Polymorphismen von TRAF1 untersucht, die sich jedoch als nicht mit der KHK assoziiert erwiesen. Darüber hinaus wurden die RNA-Expressionen der TRAFs in einer Korrelationsanalyse ausgewertet, wodurch gezeigt werden konnte, dass im Menschen zwischen TRAF2, -3, -4, -5 und -7 Zusammenhänge bestehen.
Alcohol consumption is a major global risk factor for mortality and morbidity. Much discussion has revolved around the diverse findings on the complex relationship between alcohol consumption and the leading cause of death and disability, ischemic heart disease (IHD).
We conducted a systematic search of the literature up to August 2014 using Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines to identify meta-analyses and observational studies examining the relationship between alcohol drinking, drinking patterns, and IHD risk, in comparison to lifetime abstainers. In a narrative review we have summarized the many meta-analyses published in the last 10 years, discussing the role of confounding and experimental evidence. We also conducted meta-analyses examining episodic heavy drinking among on average moderate drinkers.
The narrative review showed that the use of current abstainers as the reference group leads to systematic bias. With regard to average alcohol consumption in relation to lifetime abstainers, the relationship is clearly J-shaped, supported by short-term experimental evidence and similar associations within strata of potential confounders, except among smokers. Women experience slightly stronger beneficial associations and also a quicker upturn to a detrimental effect at lower levels of average alcohol consumption compared to men. There was no evidence that chronic or episodic heavy drinking confers a beneficial effect on IHD risk. People with alcohol use disorder have an elevated risk of IHD (1.5- to 2-fold). Results from our quantitative meta-analysis showed that drinkers with average intake of <30 g/day and no episodic heavy drinking had the lowest IHD risk (relative risk = 0.64, 95% confidence interval 0.53 to 0.71). Drinkers with episodic heavy drinking occasions had a risk similar to lifetime abstainers (relative risk = 1.12, 95% confidence interval 0.91 to 1.37).
Epidemiological evidence for a beneficial effect of low alcohol consumption without heavy drinking episodes is strong, corroborated by experimental evidence. However, episodic and chronic heavy drinking do not provide any beneficial effect on IHD. Thus, average alcohol consumption is not sufficient to describe the risk relation between alcohol consumption and IHD. Alcohol policy should try to reduce heavy drinking patterns.
Background:
Studies investigating the role of alcohol consumption in the development of abdominal aortic aneurysm (AAA) are scarce. We aimed to examine associations between total alcohol consumption and specific alcoholic beverages and the hazard of AAA.
Methods and results:
The study population was made up of 44 715 men from the Cohort of Swedish Men and 35 569 women from the Swedish Mammography Cohort who were 46 to 84 years of age at baseline in 1998. Cox proportional hazards models were used to estimate hazard ratios with 95% confidence intervals for the associations between alcohol consumption, assessed through a food frequency questionnaire, and AAA, identified by means of linkage to the Swedish Inpatient Register and the Swedish Vascular Registry (Swedvasc). Over the 14-year follow-up until December 2011 (1 019 954 person-years), AAAs occurred in 1020 men and 194 women. Compared with the consumption of 1 glass of alcohol per week (12 g of ethanol), the hazard ratio of AAA among men who consumed 10 glasses per week was 0.80 (95% confidence interval, 0.68-0.94). The corresponding hazard ratio among women who consumed 5 glasses per week was 0.57 (95% confidence interval, 0.40-0.82). Among participants free from cardiovascular disease, total alcohol consumption did not seem to be associated with hazard of the disease. The most commonly consumed alcoholic beverages, beer among men and wine among women, were inversely associated, whereas no association was observed for liquor.
Conclusions:
Moderate alcohol consumption, specifically wine and beer, was associated with a lower hazard of abdominal aortic aneurysm. The associations between higher doses of alcohol and risk of the disease remain unknown.
Low to moderate alcohol intake has been associated with beneficial effects on the heart and the vasculature, including improvements in several established and emerging cardiovascular disease (CVD) risk factors as well as reduced risk for several metabolic diseases, CVD morbidity and mortality. Binge and heavy drinking exert the opposite effects, leading to increased risks for all the above conditions. With regard to beverage type, there is some evidence supporting red wine superiority in cardioprotection, although other beverages have also been reported to exert beneficial metabolic and vascular effects when consumed in moderate amounts. In this narrative review we discuss the associations between alcohol consumption and CVD morbidity and mortality. Alcohol-induced effects on established and emerging CVD risk factors are also discussed taking into consideration different drinking patterns. Physicians should screen for excessive alcohol use and advise individuals to limit their alcohol intake to moderate amounts (up to 20-30 g/day for men and 10-20 g/day for women), preferably consumed with meals. The question of whether alcohol intake should be encouraged as a measure to prevent CVD remains unanswered.
It is well known that light to moderate drinking (10-25 g/day) has a protective effect on ischaemic heart disease. This effect seems independent of the type of alcoholic beverage. Recently, the International Agency for Research on Cancer (World Health Organization) stated that alcoholic beverages are carcinogenic for human (oral cavity, pharynx, larynx, oesophagus, colorectum, liver and breast). There is a dose-response relationship between alcohol and cancer in that the risk of cancer increases proportionally with alcohol consumption. Low doses of alcohol (10 g/day) are associated with an increased risk for oral cavity, pharynx, larynx, oesophagus and breast cancer. Therefore, a physically active lifestyle and a healthy diet are more effective in preventing ischaemic heart disease than a low level of alcohol consumption.
Since its advent, alcohol has been utilized throughout history socially, for rituals, worship, and for its therapeutic, antibacterial, and analgesic properties. In moderation, alcohol consumption and its use are generally viewed as clinically beneficial. Excessive alcohol consumption on the other hand has been recognized as having several adverse implications. Excessive use increases the risk of liver and heart disease, metabolic disturbances, nutritional deficiencies, certain cancers, brain damage, dementia, neuropathy, as well as other facets of morbidity and mortality. This review targets the sequelae of alcohol consumption on the heart, specifically on myocardial contractility, calcium channel signaling, and intracellular signaling pathways. With the incidence of alcohol-induced cardiac abnormalities being higher than previously thought, it is of increasing importance to elucidate the mechanisms behind them. Here, the cardiac effects of alcohol were not discussed in isolation but in conjunction with other important factors, such as high- and low-density lipoprotein levels and vascular dilatory influences. We explore these mechanisms, in particular, the oxidative stress as the major contributor, as well as pathways that may prove to be cardioprotective. As such, we demonstrate the involvement of nuclear factor (erythroid-derived 2)-like 2 (NFE2L2/NRF2) as well as AKT that act as regulators of oxidative balance during oxidative stress responses. Thus, alcohol consumption may confer a cardioprotective effect when used in moderation through an AKT/NRF2-dependent mechanism.
Background and purpose:
Approximately 5% of strokes occur in adults aged 18 to 44 years. Substance abuse is a prevalent risk factor for stroke in young adults. We sought to identify trends in substance abuse detection among stroke patients.
Methods:
Using a population-based design, we sought to identify all patients aged 18 to 54 years experiencing a stroke (ischemic or hemorrhagic) in the Greater Cincinnati and Northern Kentucky Study region during 1993 to 1994, 1999, and 2005. Demographic and clinical characteristics and substance use data were obtained retrospectively from chart review and adjudicated by physicians.
Results:
The number of young patients identified with a stroke increased from 1993 to 1994 (297) to 2005 (501). Blacks (61% vs 51%; P<0.02) and men (61% vs 47%; P<0.002) reported substance abuse (current smoking, alcohol, or illegal drug use) more frequently than did whites and women. Overall use of substances increased across study periods, 45% in 1993 versus 62% in 2005 (P=0.003). The trend was significant for illegal drug use (3.8% in 1993 vs 19.8% in 2005) and ever smoking (49% in 1993 vs 66% in 2005). Documentation of both cocaine and marijuana use increased over time. In 2005, half of young adults with a stroke were current smokers, and 1 in 5 abused illegal drugs.
Conclusions:
Substance abuse is common in young adults experiencing a stroke. The observed increase in substance abuse is contributing to the increased incidence of stroke in young adults. Patients aged younger than 55 years who experience a stroke should be routinely screened and counseled regarding substance abuse.
The aim of this narrative review is to assess the potential association between arterial and venous thrombotic events. Several studies have suggested that the major cardiovascular risk factors, alone or in combination (e.g. in the metabolic syndrome), are significantly associated with venous thromboembolism (VTE). Recent evidence also suggests that microalbuminuria and non-alcoholic liver steatosis, both markers of arterial disease, may independently predict the risk for VTE. An association between a history of VTE and the risk of future arterial events is also well documented, inflammation and endothelial dysfunction being thought as the common soil on which further investigation in the area should be pursued. The existence of a common pathophysiologic background is also suggested by the evidence that aspirin, low-molecular weight heparin (LMWH) and warfarin are recommended for the prevention and treatment of both venous and arterial thrombosis. In addition, rosuvastatin recently has been shown to prevent venous thromboembolism (VTE) in a time-dependent fashion. Together, these data argue for patients with a history of VTE as being at intermediate/high cardiovascular risk, a concept that implies that VTE patients should undergo a careful assessment for the presence of cardiovascular risk factors and adequate lifestyle changes. The value of routine screening for asymptomatic atherosclerosis (e.g. 2D echocardiography, microalbuminuria, arterial vessel ultrasonography) in these patients should be confirmed in future studies.
Background:
Moderate consumption of alcohol is inversely related with coronary disease, but its association with mortality is controversial. We performed a meta-analysis of prospective studies on alcohol dosing and total mortality.
Methods:
We searched PubMed for articles available until December 2005, supplemented by references from the selected articles. Thirty-four studies on men and women, for a total of 1 015 835 subjects and 94 533 deaths, were selected. Data were pooled with a weighed regression analysis of fractional polynomials.
Results:
A J-shaped relationship between alcohol and total mortality was confirmed in adjusted studies, in both men and women. Consumption of alcohol, up to 4 drinks per day in men and 2 drinks per day in women, was inversely associated with total mortality, maximum protection being 18% in women (99% confidence interval, 13%-22%) and 17% in men (99% confidence interval, 15%-19%). Higher doses of alcohol were associated with increased mortality. The inverse association in women disappeared at doses lower than in men. When adjusted and unadjusted data were compared, the maximum protection was only reduced from 19% to 16%. The degree of association in men was lower in the United States than in Europe.
Conclusions:
Low levels of alcohol intake (1-2 drinks per day for women and 2-4 drinks per day for men) are inversely associated with total mortality in both men and women. Our findings, while confirming the hazards of excess drinking, indicate potential windows of alcohol intake that may confer a net beneficial effect of moderate drinking, at least in terms of survival.
In the 1980s, observational retrospective studies showed an inverse relation between coronary heart disease (CHD) and consumption of fish containing fatty acids that belong to the omega (ω)-3 family. Large case-control studies and prospective intervention trials consistently showed that ω-3 fatty acids supplementation lowers fatal myocardial infarction (MI) and sudden cardiac death. By analysing the strengths of the results of individual studies and how the meta-analyses agree with them, putting together relevant backgrounds, and identifying open questions, the following findings/directions emerge. (i) Dietary and non-dietary intake of ω-3 fatty acids reduces overall mortality, mortality due to MI, and sudden death in patients with CHD; (ii) Fish oil consumption directly or indirectly affects cardiac electrophysiology. Fish oil reduces heart rate, a major risk factor for sudden death; (iii) Among patients with implantable cardioverter defibrillators, ω-3 fatty acids do not reduce the risk of ventricular tachycardia/ventricular fibrillation and may actually be pro-arrhythmic; (iv) The consumption of ω-3 fatty acids leads to a 10-33% net decrease of triglyceride levels. The effect is dose-dependent, larger in studies with higher mean baseline triglyceride levels, and consistent in different populations (healthy people, people with dyslipidaemia, diabetes, or known cardiovascular risk factors); (v) Outcomes for which a small beneficial effect ω-3 fatty acids is found include blood pressure (about 2 mmHg reduction), re-stenosis rates after coronary angioplasty (14% reduction), and exercise tolerance testing. Major experimental data provide strength (biological plausibility) for these findings, and define directions for newer clinical trials with ω-3 fatty acids.
The term FRENCH PARADOX was coined in 1992 to describe the relatively low incidence of cardiovascular disease in the French population, despite a relatively high dietary intake of saturated fats, and potentially attributable to the consumption of red wine. After nearly 20 years, several studies have investigated the fascinating, overwhelmingly positive biological and clinical associations of red wine consumption with cardiovascular disease and mortality. Light to moderate intake of red wine produces a kaleidoscope of potentially beneficial effects that target all phases of the atherosclerotic process, from atherogenesis (early plaque development and growth) to vessel occlusion (flow-mediated dilatation, thrombosis). Such beneficial effects involve cellular signaling mechanisms, interactions at the genomic level, and biochemical modifications of cellular and plasma components. Red wine components, especially alcohol, resveratrol, and other polyphenolic compounds, may decrease oxidative stress, enhance cholesterol efflux from vessel walls (mainly by increasing levels of high-density lipoprotein cholesterol), and inhibit lipoproteins oxidation, macrophage cholesterol accumulation, and foam-cell formation. These components may also increase nitric oxide bioavailability, thereby antagonizing the development of endothelial dysfunction, decrease blood viscosity, improve insulin sensitivity, counteract platelet hyperactivity, inhibit platelet adhesion to fibrinogen-coated surfaces, and decrease plasma levels of von Willebrand factor, fibrinogen, and coagulation factor VII. Light to moderate red wine consumption is also associated with a favorable genetic modulation of fibrinolytic proteins, ultimately increasing the surface-localized endothelial cell fibrinolysis. Overall, therefore, the "French paradox" may have its basis within a milieu containing several key molecules, so that favorable cardiovascular benefits might be primarily attributable to combined, additive, or perhaps synergistic effects of alcohol and other wine components on atherogenesis, coagulation, and fibrinolysis. Conversely, chronic heavy alcohol consumption and binge drinking are associated with increased risk of cardiovascular events. In conclusion, although mounting evidence strongly supports beneficial cardiovascular effects of moderate red wine consumption (one to two drinks per day; 10-30 g alcohol) in most populations, clinical advice to abstainers to initiate daily alcohol consumption has not yet been substantiated in the literature and must be considered with caution on an individual basis.
With the exception of breast cancer, little is known about the effect of moderate intakes of alcohol, or of particular types of alcohol, on cancer risk in women.
A total of 1,280,296 middle-aged women in the United Kingdom enrolled in the Million Women Study were routinely followed for incident cancer. Cox regression models were used to calculate adjusted relative risks and 95% confidence intervals (CIs) for 21 site-specific cancers according to amount and type of alcoholic beverage consumed. All statistical tests were two-sided.
A quarter of the cohort reported drinking no alcohol; 98% of drinkers consumed fewer than 21 drinks per week, with drinkers consuming an average of 10 g alcohol (1 drink) per day. During an average 7.2 years of follow-up per woman 68,775 invasive cancers occurred. Increasing alcohol consumption was associated with increased risks of cancers of the oral cavity and pharynx (increase per 10 g/d = 29%, 95% CI = 14% to 45%, Ptrend < .001), esophagus (22%, 95% CI = 8% to 38%, Ptrend = .002), larynx (44%, 95% CI = 10% to 88%, Ptrend = .008), rectum (10%, 95% CI = 2% to 18%, Ptrend = .02), liver (24%, 95% CI = 2% to 51%, Ptrend = .03), breast (12%, 95% CI = 9% to 14%, Ptrend < .001), and total cancer (6%, 95% CI = 4% to 7%, Ptrend < .001). The trends were similar in women who drank wine exclusively and other consumers of alcohol. For cancers of the upper aerodigestive tract, the alcohol-associated risk was confined to current smokers, with little or no effect of alcohol among never and past smokers (P(heterogeneity) < .001). Increasing levels of alcohol consumption were associated with a decreased risk of thyroid cancer (Ptrend = .005), non-Hodgkin lymphoma (Ptrend = .001), and renal cell carcinoma (Ptrend = .03).
Low to moderate alcohol consumption in women increases the risk of certain cancers. For every additional drink regularly consumed per day, the increase in incidence up to age 75 years per 1000 for women in developed countries is estimated to be about 11 for breast cancer, 1 for cancers of the oral cavity and pharynx, 1 for cancer of the rectum, and 0.7 each for cancers of the esophagus, larynx and liver, giving a total excess of about 15 cancers per 1000 women up to age 75.
To investigate the association between treatment induced change in high density lipoprotein cholesterol and total death, coronary heart disease death, and coronary heart disease events (coronary heart disease death and non-fatal myocardial infarction) adjusted for changes in low density lipoprotein cholesterol and drug class in randomised trials of lipid modifying interventions.
Systematic review and meta-regression analysis of randomised controlled trials.
Medline, Embase, Central, CINAHL, and AMED to October 2006 supplemented by contact with experts in the field.
In teams of two, reviewers independently determined eligibility of randomised trials that tested lipid modifying interventions to reduce cardiovascular risk, reported high density lipoprotein cholesterol and mortality or myocardial infarctions separately for treatment groups, and treated and followed participants for at least six months.
Using standardised, pre-piloted forms, reviewers independently extracted relevant information from each article. The change in lipid concentrations for each trial and the weighted risk ratios for clinical outcomes were calculated.
The meta-regression analysis included 108 randomised trials involving 299 310 participants at risk of cardiovascular events. All analyses that adjusted for changes in low density lipoprotein cholesterol showed no association between treatment induced change in high density lipoprotein cholesterol and risk ratios for coronary heart disease deaths, coronary heart disease events, or total deaths. With all trials included, change in high density lipoprotein cholesterol explained almost no variability (<1%) in any of the outcomes. The change in the quotient of low density lipoprotein cholesterol and high density lipoprotein cholesterol did not explain more of the variability in any of the outcomes than did the change in low density lipoprotein cholesterol alone. For a 10 mg/dl (0.26 mmol/l) reduction in low density lipoprotein cholesterol, the relative risk reduction was 7.2% (95% confidence interval 3.1% to 11%; P=0.001) for coronary heart disease deaths, 7.1% (4.5% to 9.8%; P<0.001) for coronary heart disease events, and 4.4% (1.6% to 7.2%; P=0.002) for total deaths, when adjusted for change in high density lipoprotein cholesterol and drug class.
Available data suggest that simply increasing the amount of circulating high density lipoprotein cholesterol does not reduce the risk of coronary heart disease events, coronary heart disease deaths, or total deaths. The results support reduction in low density lipoprotein cholesterol as the primary goal for lipid modifying interventions.
The effect of alcohol drinking on LDL-cholesterol concentrations is unclear. The reported variability may be due to interactions between genetic factors and alcohol intake.
The purpose of the study was to examine whether variation at the apolipoprotein E gene (APOE) locus modulates the association between alcohol drinking and LDL cholesterol.
We used a cross-sectional design in a healthy population-based sample of 1014 men and 1133 women from the Framingham Offspring Study.
In male nondrinkers (n = 197), LDL cholesterol was not significantly different across APOE allele groups [APOE*E2 (E2), APOE*E3 (E3), and APOE*E4 (E4)]. However, in male drinkers (n = 817), differences were observed (P: < 0.001); those with the E2 allele had the lowest concentrations. LDL cholesterol in men with the E2 allele was significantly lower in drinkers than in nondrinkers but was significantly higher in drinkers than in nondrinkers in men with the E4 allele. This APOE-alcohol interaction remained significant (P < 0.001) after age, body mass index, smoking status, and fat and energy intakes were controlled for. In women, the expected effect of APOE alleles on LDL cholesterol occurred in both drinkers (n = 791; P < 0.001) and nondrinkers (n = 342; P < 0.001). Multiple linear regression models showed a negative association (P < 0.05) between alcohol and LDL cholesterol in men with the E2 allele but a positive association in men with the E4 allele. No significant associations were observed in men or women with the E3 allele.
In men, the effects of alcohol intake on LDL cholesterol are modulated in part by variability at the APOE locus.
Moderate alcohol consumption is associated with a reduced risk of cardiovascular disease. Data on alcohol consumption and atherosclerosis are scarce. To determine the association between alcohol consumption and risk of peripheral arterial disease, the authors carried out a cross-sectional study (1990-1993) in the population-based Rotterdam Study among men and women aged 55 years or over. Data on alcohol consumption and peripheral arterial disease, as measured by the ankle/brachial blood pressure index, were available for 3,975 participants without symptomatic cardiovascular disease. Male drinkers consumed beer, wine, and liquor, while female drinkers consumed predominantly wine and fortified wine types. An inverse relation between moderate alcohol consumption and peripheral arterial disease was found in women but not in men. Because of residual confounding by smoking, analyses were repeated in nonsmokers. In nonsmoking men, odds ratios were 0.86 (95% confidence interval (CI): 0.46, 1.63) for daily alcohol consumption up to and including 10 g, 0.75 (95% CI: 0.37, 1.55) for 11-20 g, and 0.68 (95% CI: 0.35, 1.34) for more than 20 g, compared with nondrinking. In nonsmoking women, corresponding odds ratios were 0.65 (95% CI: 0.48, 0.87), 0.66 (95% CI: 0.42, 1.05), and 0.41 (95% CI: 0.21, 0.77), respectively. In conclusion, an inverse association between alcohol consumption and peripheral arterial disease was found in nonsmoking men and women.
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.
The purpose of this study was to quantify the relation between alcohol consumption and cardiovascular and total mortality in patients with a history of cardiovascular events.
Regular, moderate alcohol consumption by healthy people is associated with lower cardiovascular and all-cause mortality. No extensive meta-analysis is presently available on the possible association of alcohol consumption with secondary events in patients with cardiovascular disease.
Articles were retrieved through October 2009 by search in PubMed and EMBASE. Fifty-four publications were identified, but only 8 were selected for our analyses, including 16,351 patients with a history of cardiovascular disease. Secondary events were cardiovascular or all-cause mortality. All selected studies were prospective. Data were pooled with a weighted, least-squares regression analysis of second-order fractional polynomial models.
The meta-analysis on cardiovascular mortality showed a J-shaped pooled curve with a significant maximal protection (average 22%) by alcohol at approximately 26 g/day. In the meta-analysis on mortality for any cause, J-shaped pooled curves were observed in the overall analysis (average maximal protection of 18% in the range of 5 to 10 g/day) and in all subgroups according to either the type of patients or the characteristics of the studies.
In patients with cardiovascular disease, light to moderate alcohol consumption (5 to 25 g/day) was significantly associated with a lower incidence of cardiovascular and all-cause mortality.
An inverse association between moderate alcohol intake and cardiovascular risk, in particular coronary disease and ischemic stroke, has been shown in many epidemiologic studies. In addition, several other diseases are also known to occur less frequently in moderate drinkers than in non-drinkers, whereas excess of drinking is invariably harmful. However, some concern has been recently raised about the possibility that at all dosages the harm of alcohol could overcome its beneficial effects. We present here the epidemiologic and mechanistic evidence to support the protective effect of moderate alcohol intake against cardiovascular disease and all-cause mortality.
The substantial medical risks of heavy alcohol drinking as well as the probable existence of a less harmful or safe drinking limit have been evident for centuries. Modern epidemiology studies suggest lowered risk of morbidity and mortality among lighter drinkers. Thus, defining "heavy" drinking as > or =3 standard drinks per day, the alcohol-mortality relationship is a J-curve with risk highest for heavy drinkers, lowest for light drinkers and intermediate for abstainers. A number of non-cardiovascular and cardiovascular problems contribute to the increased mortality risk of heavier drinkers. The lower risk of light drinkers is due mostly to lower risk of the most common cardiovascular condition, coronary heart disease (CHD). These disparate relationships of alcoholic drinking to various cardiovascular and non-cardiovascular conditions constitute a modern concept of alcohol and health. Increased cardiovascular risks of heavy drinking include: (1) alcoholic cardiomyopathy, (2) systemic hypertension (high blood pressure), (3) heart rhythm disturbances, and (4) hemorrhagic stroke. Lighter drinking is not clearly related to increased risk of any cardiovascular condition and, in observational studies, is related to lower risk of CHD, ischemic stroke, and diabetes mellitus. A protective hypothesis for CHD is supported by evidence for plausible biological mechanisms attributable to ethyl alcohol. International comparisons and some prospective study data suggest that wine is more protective against CHD than liquor or beer. Possible non-alcohol beneficial components in wine (especially red) support possible extra protection by wine, but a healthier pattern of drinking or more favorable risk traits in wine drinkers may be involved.
Several studies have shown that moderate alcohol consumption reduces the risk of coronary heart disease, a disease related to oxidative stress. However, the effects of different alcoholic beverages on antioxidant status are not fully known. Our aim was therefore to compare the effects of a moderate intake of an alcoholic beverage with high polyphenol content (red wine) and another without polyphenol content (gin) on plasma antioxidant vitamins, lipid profile and oxidability of low-density lipoprotein (LDL) particles.
Forty healthy men (mean age, 38 years) were included in a randomised cross-over trial. After a 15-day washout period, subjects received 30 g/ethanol/d as either wine or gin for 28 days. Diet and exercise were monitored. Before and after each intervention, we measured serum vitamins, malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase activities, lipid profile, oxidized LDL and LDL resistance to ex-vivo oxidative stress. Compared to gin intervention, wine intake reduced plasma SOD activity [-8.1 U/gHb (95% confidence interval, CI, -138 to -25; P=0.009)] and MDA levels [-11.9 nmol/L (CI, -21.4 to-2.5; P=0.020)]. Lag phase time of LDL oxidation analysis also increased 11.0 min (CI, 1.2-20.8; P=0.032) after wine, compared to gin, whereas no differences were observed between the two interventions in oxidation rate of LDL particles. Peroxide concentration in LDL particles also decreased after wine [-0.18 nmol/mL (CI, -0.3 to-0.08;P=0.020)], as did plasma oxidized LDL concentrations [-11.0 U/L (CI,-17.3 to -6.1; P=0.009)].
Compared to gin, red wine intake has greater antioxidant effects, probably due to its high polyphenolic content.
Alcohol consumption has been identified as an important risk factor for chronic disease and injury. In the first paper in this Series, we quantify the burden of mortality and disease attributable to alcohol, both globally and for ten large countries. We assess alcohol exposure and prevalence of alcohol-use disorders on the basis of reviews of published work. After identification of other major disease categories causally linked to alcohol, we estimate attributable fractions by sex, age, and WHO region. Additionally, we compare social costs of alcohol in selected countries. The net effect of alcohol consumption on health is detrimental, with an estimated 3.8% of all global deaths and 4.6% of global disability-adjusted life-years attributable to alcohol. Disease burden is closely related to average volume of alcohol consumption, and, for every unit of exposure, is strongest in poor people and in those who are marginalised from society. The costs associated with alcohol amount to more than 1% of the gross national product in high-income and middle-income countries, with the costs of social harm constituting a major proportion in addition to health costs. Overall, we conclude that alcohol consumption is one of the major avoidable risk factors, and actions to reduce burden and costs associated with alcohol should be urgently increased.
Previous studies suggest that consuming moderate to high amounts of alcohol on a regular basis might increase the risk of developing atrial fibrillation in men but not in women. However, these studies were not powered to investigate the association of alcohol consumption and atrial fibrillation among women.
To prospectively assess the association between regular alcohol consumption and incident atrial fibrillation among women.
Participants were 34 715 initially healthy women participating in the Women's Health Study, a completed randomized controlled trial conducted in the United States. Participants were older than 45 years and free of atrial fibrillation at baseline and underwent prospective follow-up from 1993 to October 31, 2006. Alcohol consumption was assessed via questionnaires at baseline and at 48 months of follow-up and was grouped into 4 categories (0, > 0 and < 1, > or = 1 and < 2, and > or = 2 drinks per day). Atrial fibrillation was self-reported on the yearly questionnaires and subsequently confirmed by electrocardiogram and medical record review.
Time to first episode of atrial fibrillation.
Over a median follow-up of 12.4 years, 653 cases of incident atrial fibrillation were confirmed. Age-adjusted incidences among women consuming 0 (n = 15,370), more than 0 and less than 1 (n = 15,758), 1 or more and less than 2 (n = 2228), and 2 or more (n = 1359) drinks per day were 1.59, 1.55, 1.27, and 2.25 events/1000 person-years of follow-up. Thus, compared with nondrinking women, women consuming 2 or more drinks per day had an absolute risk increase of 0.66 events/1000 person-years. The corresponding multivariate-adjusted hazard ratios (HRs) for incident atrial fibrillation were 1, 1.05 (95% CI, 0.88-1.25), 0.84 (95% CI, 0.58-1.22), and 1.60 (95% CI, 1.13-2.25), respectively. The increased hazard in the small group of women consuming 2 or more drinks per day persisted when alcohol intake was updated at 48 months (HR, 1.49; 95% CI, 1.05-2.11) or when women were censored at their first cardiovascular event (HR, 1.68; 95% CI, 1.18-2.39).
Among healthy middle-aged women, consumption of up to 2 alcoholic beverages per day was not associated with an increased risk of incident atrial fibrillation. Heavier consumption of 2 or more drinks per day, however, was associated with a small but statistically significant increased risk of atrial fibrillation.
From the Department of Cell Biology, Neurobiology & Anatomy (MAC, EJN), Loyola University Chicago Stritch School of Medicine, Maywood, Illinois; the Division of General Medicine and Primary Care (KJM), Beth Israel Deaconess Medical Center, Boston, Massachusetts; the Division of Cardiology (MOG), San Francisco General Hospital, San Francisco, California; the Center for Wine and Cardiovascular Health (DAP), University of Alabama, Birmingham, Alabama; the Cardiovascular Research Center (DKD), University of Connecticut School of Medicine, Farmington, Connecticut; and the Department of Medical Pharmacology and Physiology (RJK), University of Missouri School of Medicine, Columbia, Missouri.
An association between excessive alcohol use and cardiac rhythm disorders is often difficult to establish in the absence of overt cardiomyopathy. We studied 32 separate hospital admissions for dysrhythmias in 24 patients (20 men, 4 women) with heavy recent alcohol ingestion and prolonged excessive alcohol use. None had evidence of overt heart disease after treatment of arrhythmia. Episodes usually followed heavy weekend or holiday sprees, resulting in hospitalization between Sunday and Tuesday or in proximity to the year-end holidays, a relationship not observed in other alcohol-associated illnesses. Atrial fibrillation was most common, but atrial flutter, atrial tachycardia, junctional tachycardia, multiple APC's, multiple PVC's and ventricular tachycardia were also observed. Transient hypokalemia was present in four of 30. The mean ratio after treatment was 0.412 ± 0.014 (normal 0.299 ± 0.008, P < 0.001). High-speed ECG's showed prolongation of PRc, QRS, and QTc. At cardiac catheterization, intracardiac pressures and volumes, coronary arteriograms and ventricular wall motion were normal at rest and mean cardiac index was slightly low, but the left ventricular response to angiotensin was abnormal. Cardiac arrhythmias presenting during weekend or holiday drinking episodes are associated with conduction delays and depressed cardiac performance indicative of early cardiomyopathy and suggest a “holiday heart” syndrome.
We studied blood pressure in relation to known drinking habits of 83,947 men and women of three races (83.5 per cent white). Using health-check-up questionnaire responses, we classified persons as nondrinkers or according to usual daily number of drinks: two or fewer per day, three to five per day, or six or more per day. As compared to nondrinkers blood pressures of men taking two or fewer drinks per day were similar. Women who took two or fewer drinks per day had slightly lower pressures. Men and women who took three or more drinks per day had higher systolic pressures (P less than 10(-24) in white men, and less than 10(-12) in white women), higher diastolic pressures (P less than 10(-24) in white men, and less than 10(-6) in white women), and substantially higher prevalence of pressures greater than or equal to 160/95 mm Hg. The associations of blood pressure and drinking were independent of age, sex, race, smoking, coffee use, former "heavy" drinking, educational attainment and adiposity. The findings strongly suggest that regular use of three or more drinks of alcohol per day is a risk factor for hypertension.
We have examined the independent and combined effects on blood pressure and blood lipids of alcohol restriction and weight loss in overweight male drinkers with a view to assessing overall effects on cardiovascular risk of two widely promoted nonpharmacological approaches for hypertension. Eighty-six men with a mean age of 44.3 years, a mean regular alcohol intake of 440 ml/wk (five or six standard drinks per day), a mean blood pressure of 137.4 mm Hg systolic and 84.8 mm Hg diastolic, and a mean body mass of 92.5 kg entered a controlled two-way factorial study. The subjects were randomly assigned to four groups for an 18-week intervention in which members of two groups drank only low-alcohol beer, thereby reducing their alcohol intake by 374 ml/wk, while those of the other two groups continued their normal alcohol intake. Within the low and normal alcohol intake groups subjects either continued their usual diet or reduced their caloric intake by 4,200-6,300 kJ/day (1,000-1,500 kcal/day) (with protein, fat, and carbohydrate provided as 15%, 30%, and 55% of total calories, respectively). Calorie reduction and alcohol restriction caused weight losses of 7.5 (p less than 0.001) and 2.1 (p less than 0.01) kg, respectively. Calorie reduction and alcohol restriction were associated with decreases in systolic blood pressure of 5.4 (p less than 0.001) and 4.8 (p less than 0.01) mm Hg, respectively, and in diastolic blood pressure of 4.2 (p less than 0.001) and 3.3 (p less than 0.01) mm Hg, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Although an inverse association between alcohol consumption and risk of coronary artery disease has been consistently found in several types of studies, some have argued that the association is due at least partly to the inclusion in the non-drinking reference group of men who abstain because of pre-existing disease. The association between self-reported alcohol intake and coronary disease was studied prospectively among 51,529 male health professionals. In 1986 the participants completed questionnaires about food and alcohol intake and medical history, heart disease risk factors, and dietary changes in the previous 10 years. Follow-up questionnaires in 1988 sought information about newly diagnosed coronary disease. 350 confirmed cases of coronary disease occurred. After adjustment for coronary risk factors, including dietary intake of cholesterol, fat, and dietary fibre, increasing alcohol intake was inversely related to coronary disease incidence (p for trend less than 0.001). Exclusion of 10,302 current non-drinkers or 16,342 men with disorders potentially related to coronary disease (eg, hypertension, diabetes, and gout) which might have led men to reduce their alcohol intake, did not substantially affect the relative risks. These findings support the hypothesis that the inverse relation between alcohol consumption and risk of coronary disease is causal.
The aim of this study was to determine whether moderate restriction of dietary salt intake leads to an additional fall in blood pressure in treated hypertensive men who are asked to simultaneously reduce their usual alcohol intake. Sixty-three subjects entered an initial 2-week familiarization period during which they continued their usual alcohol intake and commenced a "low sodium" diet (less than 60 mmol/day) supplemented with 100 mmol sodium chloride per day as enteric-coated tablets. Subjects were then randomly assigned to either drink a low alcohol beer alone for a 4-week period (reducing their self-reported alcohol consumption from 537 to 57 ml/week) or to continue their usual alcohol intake (543 versus 557 ml/week). Within the low and normal alcohol intake groups, subjects were assigned to either a low or normal sodium intake. The low sodium groups continued the sodium-restricted diet but were switched to placebo sodium chloride tablets for the 4 weeks. This resulted in a fall in the 24-hour urinary sodium excretion from 144 to 69 mmol/day. The normal sodium groups continued the low sodium diet but kept taking 100 mmol/day of the sodium chloride tablets, and their urinary sodium excretion remained unchanged (125 versus 142 mmol/day). Regular antihypertensive therapy was continued throughout. Fifty-nine subjects completed the trial. In those who reduced their alcohol intake there was a fall in both systolic blood pressure (-5.4 mm Hg supine, p less than 0.01) and diastolic blood pressure (-3.2 mm Hg supine, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
1. Seventy-two sedentary male drinkers, aged 20–45 years, and with mean blood pressure (BP) at entry of 132±1.2/73±0.9 mmHg, completed a 4 week study during which they were assigned randomly to either drink a low alcohol beer (effectively reducing their weekly alcohol intake from 481±47 mL to 52±5 mL) or to continue their normal drinking habits.
2. Within these two groups subjects were further assigned to either a moderate exercise programme of three 30 min sessions per week of stationary cycling at 60–70% maximum workload or to a control light exercise programme where they pedalled against zero or minimal resistance.
3. Both alcohol restriction and moderate exercise were associated with mean falls in bodyweight of 0.5 kg. After adjustment for bodyweight a significant main effect of alcohol restriction on systolic BP (-4.1±1.7 mmHg, P<0.05) and diastolic BP (-1.6±0.8 mmHg, P= 0.05) was demonstrated. There was no significant main effect of moderate exercise on systolic or diastolic blood pressure despite a significant improvement in physical fitness (maximal oxygen uptake increasing from 33.2±0.08 mL/kg per min to 35.5±0.1 mL/kg per min).
4. Significant falls in high density lipoprotein cholesterol (HDLC) and triglyceride levels seen with alcohol restriction were unaffected by the increase in fitness, the magnitude of the fall being similar in both the moderate and light exercise groups.
5. We conclude that in male drinkers 4 weeks of moderate exercise has no influence on serum HDLC levels and when combined with alcohol restriction does not lead to a greater fall in BP than that seen with a reduction of alcohol intake alone.
To determine the prevalence of alcoholic myopathy and cardiomyopathy, we studied a group of 50 asymptomatic alcoholic men (mean age, 38.5 years) entering an outpatient treatment program. Studies performed included an assessment of muscle strength by electronic myometer, muscle biopsy, echocardiography, and radionuclide cardiac scanning, with comparison to healthy control subjects of similar age. The patients' mean (+/- SEM) daily alcohol consumption was 243 +/- 13 g over an average of 16 years. These patients had no clinical or laboratory signs of malnutrition or electrolyte imbalance. Forty-two percent of the patients, as compared with none of the controls, had strength of less than 20 kg as measured in the deltoid muscle. Muscle-biopsy specimens from 23 patients (46 percent) had histologic evidence of myopathy. In the cardiac studies, when the alcoholic patients were compared with 20 healthy controls, the patients had a significantly lower mean ejection fraction (59 vs. 67 percent), a lower mean shortening fraction (33 vs. 38 percent), a greater mean end-diastolic diameter (51 vs. 49 mm), and a greater mean left ventricular mass (123 vs. 106 g per square meter of body-surface area). One third of the alcoholics had an ejection fraction of 55 percent or less, as compared with none of the controls. Endomyocardial biopsy specimens from six patients with ejection fractions below 50 percent showed histologic changes of cardiomyopathy. The estimated total lifetime dose of ethanol correlated inversely with muscular strength (r = -0.65; P less than 0.001). In an analysis that also included six patients with symptomatic alcoholic cardiomyopathy, the estimated total lifetime dose of ethanol correlated inversely with the ejection fraction (r = -0.58; P less than 0.001) and directly with the left ventricular mass (r = 0.59; P less than 0.001). We conclude that myopathy of skeletal muscle and cardiomyopathy are common among persons with chronic alcoholism and that alcohol is toxic to striated muscle in a dose-dependent manner.
An association of heavier alcohol ingestion with cardiac arrhythmias has been suspected for decades. The concept of the “holiday heart syndrome” (supraventricular arrhythmia [SVA] induced by drinking binges) was popularized by Ettinger et al1 10 years ago. Supporting evidence has consisted of case reports, a few case-control studies and data suggesting that alcohol potentiates arrhythmogenesis in the laboratory. Yet, the sparse available prospective data have failed to support an alcohol-SVA association. Consideration of the subject is complicated by the disparate relations between alcohol and various conditions2 that could, in turn, be related to SVA. Heavier drinking is associated with cardiomyopathy and hypertension, while coronary artery disease is more prevalent in abstainers. Considering these problems, we have attempted to study prospectively the relation of heavier alcohol intake to SVA in a large free-living population.
In 1980, 87,526 female nurses 34 to 59 years of age completed a dietary questionnaire that assessed their consumption of beer, wine, and liquor. By 1984, during 334,382 person-years of follow-up, we had documented 200 incident cases of severe coronary heart disease (164 nonfatal myocardial infarctions and 36 deaths due to coronary disease), 66 ischemic strokes, and 28 subarachnoid hemorrhages. Follow-up was 98 percent complete. As compared with nondrinkers, women who consumed 5 to 14 g of alcohol per day (three to nine drinks per week) had a relative risk of coronary disease of 0.6 (95 percent confidence interval, 0.4 to 0.9); for 15 to 24 g per day the relative risk was 0.6 (0.3 to 1.1), and for 25 g or more per day it was 0.4 (0.2 to 0.8), after adjustment for risk factors for coronary disease. Alcohol intake was also associated with a decreased risk of ischemic stroke. For 5 to 14 g of alcohol per day the relative risk was 0.3 (0.1 to 0.7), and for 15 g per day or more it was 0.5 (0.2 to 1.1). In contrast, although the number of cases of subarachnoid hemorrhage was small, alcohol intake tended to be associated with an increased risk of this disorder; for 5 to 14 g per day the relative risk was 3.7 (1.0 to 13.8). These prospective data suggest that among middle-aged women, moderate alcohol consumption decreases the risks of coronary heart disease and ischemic stroke but may increase the risk of subarachnoid hemorrhage.
A direct pressor effect of alcohol is proposed as the basis for the association between regular alcohol consumption and an increase in blood pressure found in population studies. To examine this further, a randomized controlled crossover trial of the effects of varying alcohol intake on blood pressure in 46 healthy male drinkers was conducted. From an average of 336 ml of ethanol per week, alcohol consumption was reduced by 80% for 6 weeks by drinking a low alcohol content beer alone. This reduction was associated with a significant reduction in systolic and diastolic blood pressure (p less than 0.001 and p less than 0.05 respectively). The mean difference in supine systolic blood pressure during the last 2 weeks of normal or low alcohol intake was 3.8 mm Hg, which correlated significantly with change in alcohol consumption (r = 0.53, p less than 0.001). Reduction of alcohol intake also caused a significant decrease in weight (p less than 0.001). After adjustment for weight change, an independent effect of alcohol on systolic but not diastolic blood pressure was still evident, with a 3.1 mm Hg fall predicted for a decrease in consumption from 350 ml of ethanol equivalent per week to 70 ml per week (p less than 0.01). Systolic blood pressure rose again when normal drinking habits were resumed. These results provide clear evidence for a direct and reversible pressor effect of regular moderate alcohol consumption in normotensive men and suggest that alcohol may play a major role in the genesis of early stages of blood pressure elevation.
Acetaldehyde, the end product of oxidative ethanol metabolism, contributes to alcohol-induced disease in the liver, but cannot account for damage in organs such as the pancreas, heart, or brain, where oxidative metabolism is minimal or absent; nor can it account for the varied patterns of organ damage found in chronic alcoholics. Thus other biochemical mediators may be important in the pathogenesis of alcohol-induced organ damage. Many human organs were found to metabolize ethanol through a recently described nonoxidative pathway to form fatty acid ethyl esters. Organs lacking oxidative alcohol metabolism yet frequently damaged by ethanol abuse have high fatty acid ethyl ester synthetic activities and show substantial transient accumulations of fatty acid ethyl esters. Thus nonoxidative ethanol metabolism in addition to the oxidative pathway may be important in the pathophysiology of ethanol-induced disease in humans.
In a new study controlled for many factors, we reconfirmed the relationship of higher blood pressure to alcohol use. This relationship was slightly stronger in men, whites, and persons 55 years of age or older. A slight increase in blood pressure appeared in men who drank one to two drinks daily, and a continuous increase occurred at all higher drinking levels among white men who had constant drinking habits. Among women, an increase occurred only at three or more drinks daily. The data suggest complete regression, beginning within days, of alcohol-associated hypertension upon abstinence. Blood pressure showed minor differences with beverage preference: those who preferred liquor had higher adjusted mean blood pressure than those preferring wine or beer. The results of this study contribute to the likelihood that the alcohol-blood pressure association is causal. Smoking, coffee use, and tea use showed no association with higher blood pressure. Systolic pressure showed a positive relationship to total serum calcium and an inverse relationship to serum potassium, but diastolic pressure showed little relationship to these blood constituents; the explanations include a possible direct effect on regulation of blood pressure.
Fifty seven patients with cardiomyopathy associated with alcoholism were followed for an average of 40.5 mth (range, 4 mth to 8 yr). None of the patients were treated with prolonged bed rest. During the follow up period, the clinical status improved in 15 patients (group A), was stable in 12 patients (group B), and had deteriorated in 30 patients (group C). Seventy three % of the group A patients abstained from alcohol, whereas in groups B and C only 25% and 13% of patients, respectively, abstained. These differences were significant : P < 0.03 (group A versus B) and P < 0.001 (group A versus C). The average duration of symptoms in the group A patients was 4.2 mth and was significantly (P < 0.05) shorter than that of patients in groups B and C (17 and 11.1 mth, respectively). Only 10 patients (17%), all in group A, had a return of heart size to normal. Twenty four patients (42%), all in group C, died in an average time of 36 mth; thus, a short duration of symptoms before initiation of therapy and abstention from alcohol were associated with a more favorable course.
The effect of alcohol on blood-pressure was studied in 16 men with hypertension who regularly drank up to 80 g of alcohol daily. Antihypertensive treatment was stopped 2 weeks before the men were admitted to hospital for a 7-day study. Blood pressure remained high in 8 patients who continued their regular alcohol consumption up to the fourth day after admission. In the next 4 days no alcohol was taken and diastolic and systolic blood pressures fell significantly. 8 other patients had no alcohol for the first 3 days after admission, but they resumed alcohol consumption from day 4 to 7. In these patients, blood pressure fell slightly after admission. Reintroduction of alcohol produced statistically significant increases in both systolic and diastolic pressures. This study demonstrated a pressor effect of alcohol in patients with hypertension and confirms the link between alcohol and blood-pressure reported in population studies. The mechanism of alcohol-induced hypertension is uncertain and is more likely to be due to an effect of alcohol rather than to the pressor response produced by alcohol withdrawal.
In many studies of diverse populations it has been found that persons drinking relatively large amounts of alcohol tend to have higher blood pressures. In the Kaiser-Permanente study of about 87,000 persons, this alcohol-blood pressure association was not attributable to demographic characteristics, adiposity, reported salt use, smoking, or coffee consumption, nor could it be explained by underreporting of alcohol consumption. If the relationship is a causal one, the pathogenesis is not yet established; direct mechanisms or the effects of withdrawal from alcohol are possible explanations. The Kaiser-Permanente data suggest that about 5% of hypertension in the general population may be due to the consumption of three or more alcoholic drinks per day. Alcohol use shows a positive relation to some sequelae of hypertension but not others; the outstanding exception is coronary heart disease which is negatively related to alcohol intake, probably through different mechanisms. In most studies, cigarette smokers have shown similar or slightly lower blood pressures than non smokers. The degree to which this is due to the thinner body build of smokers, on the average, is not well established; nor is the degree to which a stronger negative relation of smoking to blood pressure might be masked by concomitant alcohol use.
The aim of this study was to determine the relationship between alcohol consumption and occurrence of peripheral arterial disease in the general population. During 1988 in a cross sectional survey, the Edinburgh Artery Study, 1,592 men and women aged 55-74 years were selected at random from the age-sex registers of ten general practices distributed geographically and socio-economically across the city. participants were asked to recall the number of units of wine, beer and spirits consumed in the previous week and whether or not this was typical. Peripheral arterial disease was measured using the ankle brachial pressure index (ABPI). Men and women were analysed separately because of large differences in alcohol consumption. There was no association between ABPI and alcohol consumption in women but, in men, increasing alcohol consumption was associated with a higher ABPI (test for trend, p = 0.03) indicating less severe disease. This relationship was linear rather than U-shaped. In multiple regression analysis, after age-adjustment the ABPI was related to wine consumption but not beer or spirits in men (p < or = 0.01). On adjusting for age and cumulative lifetime cigarette smoking, the association of wine consumption with the ABPI was diminished but remained statistically significant (p < 0.05). On adjusting for age and social class, the relationship of total alcohol intake and wine consumption with the ABPI became non significant (p > 0.05). We conclude that in males, greater alcohol consumption is related to a higher ABPI and that any protective 'effect' of alcohol relates to wine consumption rather than beer or spirits.(ABSTRACT TRUNCATED AT 250 WORDS)
To assess whether an association exists between moderate alcohol consumption and plasma concentration of endogenous tissue-type plasminogen activator (t-PA), a serine protease that plays a central role in the regulation of intravascular fibrinolysis.
Survey of self-reported alcohol consumption and plasma fibrinolytic capacity, controlled for lipid and nonlipid cardiac risk factors.
Participants in the Physicians' Health Study.
A total of 631 apparently healthy male physicians aged 40 to 84 years with no history of myocardial infarction, stroke, or transient cerebral ischemia.
Plasma concentration of t-PA antigen.
A direct association was found between alcohol consumption and plasma level of t-PA antigen, such that mean plasma levels of t-PA antigen for daily, weekly, monthly, and rare or never drinkers were 10.9, 9.7, 9.1, and 8.1 ng/mL, respectively (P trend = .0002). The relation between alcohol consumption and t-PA antigen level was not materially changed in analyses that adjusted for total cholesterol and high-density lipoprotein cholesterol or nonlipid cardiovascular risk factors including age, body mass index, parental history of coronary heart disease, exercise frequency, and systolic and diastolic blood pressure.
These data indicate a positive association between moderate alcohol intake and plasma level of endogenous t-PA antigen that is independent of high-density lipoprotein cholesterol. This finding supports the hypothesis that changes in fibrinolytic potential may be an important mechanism whereby moderate alcohol consumption decreases risk of heart disease.
Previous studies have suggested that moderate alcohol intake exerts a protective effect against coronary heart disease. Alterations in plasma lipoprotein levels represent one plausible mechanism of this apparent protective effect.
We therefore examined the interrelation among alcohol consumption, plasma lipoprotein levels, and the risk of myocardial infarction in 340 patients who had had myocardial infarctions and an equal number of age- and sex-matched controls. The case patients were men or women less than 76 years of age with no history of coronary disease who were discharged from one of six hospitals in the Boston area with a diagnosis of a confirmed myocardial infarction. Alcohol consumption was estimated by means of a food-frequency questionnaire.
We observed a significant inverse association between alcohol consumption and the risk of myocardial infarction (P for trend, < 0.001 after control for known coronary risk factors). In multivariate analyses, the relative risk for the highest intake category (subjects who consumed three or more drinks per day) as compared with the lowest (those who had less than one drink a month) was 0.45 (95 percent confidence interval, 0.26 to 0.80). The levels of total high-density lipoprotein cholesterol (HDL) and its HDL2 and HDL3 subfractions were strongly associated with alcohol consumption (P for trend, < 0.001 for each). The addition of HDL or either of its subfractions to the multivariate model substantially reduced the inverse association between alcohol intake and myocardial infarction, whereas the addition of the other plasma lipid measurements did not materially alter the relation.
These data confirm the inverse association of moderate alcohol intake with the risk of myocardial infarction and support the view that the effect is mediated, in large part, by increases in both HDL2 and HDL3.
To test the hypothesis that red wine, by virtue of its relatively high concentration of polyphenols, is more protective against atherosclerosis and coronary heart disease (CHD) than white wine, and that grape juice enriched in one of these, trans-resveratrol, may share some of these properties, studies were performed on 24 healthy males aged 26-45 years. Each consumed the following beverages for periods of 4 weeks: red wine, white wine, commercial grape juice and the same grape juice enriched with trans-resveratrol. Apart from the last beverage, 2 weeks abstinence was maintained before commencing the schedule. Blood was taken at the beginning and end of each schedule to determine plasma thromboxane B2 (TxB2) concentration and the IC50 (concentration required for 50% aggregation) for ADP and thrombin-induced platelet aggregation. White wine (P < 0.05) but not red wine increased the IC50 for ADP. Both wines increased the IC50 for thrombin (P < 0.02 and P < 0.001, respectively) and also lowered plasma TxB2 concentrations (P < 0.01 and P < 0.025, respectively). Neither grape juice altered ADP-induced aggregation or TxB2 concentrations, but the commercial juice lowered the IC50 for thrombin (P < 0.001) whereas the resveratrol-enriched juice caused a dramatic increase (P < 0.001). In vitro experiments demonstrated that the aggregation of fresh washed human platelets by ADP and thrombin was moderately reduced by both grape juices, strongly by red wine and not at all by white wine. The synthesis of TxB2 by platelets from labelled arachidonate was stimulated by commercial grape juice, slightly enhanced by resveratrol-enriched juice and strongly inhibited by red wine with white wine having little effect. Platelets from subjects consuming the commercial juice had a higher ratio of cyclo-oxygenase to lipoxygenase product formation and those consuming the resveratrol-enriched juice a lower ratio than during the control period. We conclude that trans-resveratrol can be absorbed from grape juice in biologically active quantities and in amounts that are likely to cause reduction in the risk of atherosclerosis. The failure of red wines (which have a 20-fold excess of polyphenols over white wines) to show any advantage suggests that, in vivo, ethanol is the dominant anti-aggregatory component in these beverages which are more potent than grape juices in preventing platelet aggregation in humans.
Polymorphonuclear leukocytes (PMN) may contribute to the pathogenesis of acute coronary heart disease (CHD).
Epidemiological and laboratory evidence suggests that red wine, by virtue of its polyphenolic constituents, may be more effective than other alcoholic beverages in reducing the risk of CHD mortality.
The aim of the present study was to investigate the effects of trans-resveratrol (3,4′,5-trihydroxy-trans-stilbene), a polyphenol present in most red wines, on functional and biochemical responses of PMN, upon in vitro activation.
trans-Resveratrol exerted a strong inhibitory effect on reactive oxygen species produced by PMN stimulated with 1 μM formyl methionyl leucyl phenylalamine (fMLP) (IC50 1.3±0.13 μM, mean±s.e.mean), as evaluated by luminol-amplified chemiluminescence.
trans-Resveratrol prevented the release of elastase and β-glucuronidase by PMN stimulated with the receptor agonists fMLP (1 μM, IC50 18.4±1.8 and 31±1.8 μM), and C5a (0.1 μM, IC50 41.6±3.5 and 42±8.3 μM), and also inhibited elastase and β-glucuronidase secretion (IC50 37.7±7 and 25.4±2.2 μM) and production of 5-lipoxygenase metabolites leukotriene B4 (LTB4), 6-trans-LTB4 and 12-trans-epi-LTB4 (IC50 48±7 μM) by PMN stimulated with the calcium ionophore A23187 (5 μM).
trans-Resveratrol significantly reduced the expression and activation of the β2 integrin MAC-1 on PMN surface following stimulation, as revealed by FACS analysis of the binding of an anti-MAC-1 monoclonal antibody (MoAb) and of the CBRM1/5 MoAb, recognizing an activation-dependent epitope on MAC-1. Consistently, PMN homotypic aggregation and formation of mixed cell-conjugates between PMN and thrombin-stimulated fixed platelets in a dynamic system were also prevented by trans-resveratrol.
These results, indicating that trans-resveratrol interferes with the release of inflammatory mediators by activated PMN and down-regulates adhesion-dependent thrombogenic PMN functions, may provide some biological plausibility to the protective effect of red wine consumption against CHD.
British Journal of Pharmacology (1998) 123, 1691–1699; doi:10.1038/sj.bjp.0701784
There is increasing evidence implicating a dietary source of plasma lipid peroxides that become elevated in the postprandial state. This phenomenon may be a contributing factor to the correlation found between postprandial hyperlipidemia and increased risk of cardiovascular disease. Using a newly developed method for measuring lipid hydroperoxides directly in plasma, a pilot study was performed which revealed that lipid hydroperoxides are indeed elevated following a fatty meal. Lipid hydroperoxides increased within 2-4 h after the meal and returned to basal levels, corresponding to the usual postprandial hyperlipidemia. A marked suppression of postprandial hydroperoxides was found when a meal was consumed with wine, suggesting that these hydroperoxides can be formed and then absorbed during the digestive process.
Existing cholesterol guidelines aimed at preventing cardiovascular disease emphasize the role of total cholesterol (TC) and low-density lipoprotein (LDL) cholesterol in lipid management decisions, with a subsidiary role for high-density lipoprotein (HDL) cholesterol in guiding treatment and little role for triglycerides. In this article, epidemiologic evidence is reviewed relating to the independent value of lipid factors in prediction of cardiovascular disease risk, including TC, LDL cholesterol, HDL cholesterol, very-low-density lipoprotein (VLDL) cholesterol and triglycerides, LDL particle size ("pattern B"), and the TC/HDL-cholesterol ratio. Several observations are highlighted. Triglycerides appear to be an independent risk factor in specific populations. Postprandial triglycerides may be superior to fasting triglycerides as a predictor of risk. LDL particle size does not have independent predictive value after adjustment for triglycerides. Particular emphasis is placed on the observation that the single most predictive lipid factor is the TC/HDL-cholesterol ratio, which implicitly incorporates information on both LDL and triglycerides in the numerator. This is the best predictor both of outcome and of treatment benefit, and its predictive value appears to be maintained into older age. It is concluded that increasing emphasis should be placed on the TC/HDL cholesterol ratio in epidemiologic analyses and in monitoring patients on therapy for dyslipidemia.
Despite the solid evidence for thrombosis playing a key role in coronary heart disease (CHD) mortality, identifying specific haemostatic risk factors for CHD has been difficult except for fibrinogen. Excessive alcohol consumption clearly affects platelet function. Moderate alcohol consumption may affect several haemostatic factors, including fibrinogen concentration, platelet aggregability and the fibrinolytic factors tissue-type plasminogen activator and plasminogen activator inhibitor. These changes support the hypothesis that moderate alcohol beneficially affects the haemostatic balance in a way that decreases the risk of CHD mortality.
In view of conflicting prior reports, we prospectively studied associations between alcohol consumption and subsequent hospitalization for hemorrhagic stroke (HS) in 431 persons. Alcohol use was determined at examinations in 1978-1984 among 128,934 members of a prepaid health plan. Cox proportional hazards models, with 6 covariates, yielded the following multivariate relative risks (95% CI's) for HS: lifelong abstainers (ref) = 1.0, exdrinkers = 0.9 (0.5-1.5), persons drinking <1/month = 1.1 (0.8-1.4), >1/month; <1 drink/day = 0.7 (0.5-0.9), 1-2/day = 0.8 (0.6-1.1), 3-5/day = 1.0 (0.6-1.5), 6+/day = 1.9 (1.0-3.5). Relationships to alcohol were similar for subarachnoid (31% of HS) or intracerebral hemorrhage (69% of HS) and in men or women. Beverage choice (wine, beer, and liquor) was not independently related. We conclude that only heavy drinking is weakly related to increased HS risk and that light drinking need not be proscribed with respect to HS risk.
Background:
Many epidemiological studies have evaluated whether different alcoholic beverages protect against cardiovascular disease. We performed a meta-analysis of 26 studies on the relationship between wine or beer consumption and vascular risk. Methods and Results- General variance-based method and fitting models were applied to pooled data derived from 26 studies that gave a quantitative estimation of the vascular risk associated with either beverage consumption. From 13 studies involving 209 418 persons, the relative risk of vascular disease associated with wine intake was 0.68 (95% confidence interval, 0.59 to 0.77) relative to nondrinkers. There was strong evidence from 10 studies involving 176 042 persons to support a J-shaped relationship between different amounts of wine intake and vascular risk. A statistically significant inverse association was found up to a daily intake of 150 mL of wine. The overall relative risk of moderate beer consumption, which was measured in 15 studies involving 208 036 persons, was 0.78 (95% confidence interval, 0.70 to 0.86). However, no significant relationship between different amounts of beer intake and vascular risk was found after meta-analyzing 7 studies involving 136 382 persons.
Conclusions:
These findings show evidence of a significant inverse association between light-to-moderate wine consumption and vascular risk. A similar, although smaller association was also apparent in beer consumption studies. The latter finding, however, is difficult to interpret because no meaningful relationship could be found between different amounts of beer intake and vascular risk.
Studying its history generally provides insights relevant to current understanding of a subject: the health effects of alcohol consumption is no exception to this rule. Perceiving past errors in the hopes of avoiding their repetition is crucial. Because there are clear disparities in the relationships of alcohol drinking to various cardiovascular conditions, attempts to simplify the subject of alcohol and cardiovascular diseases have delayed understanding this area. Thus, the following are considered separately: cardiomyopathy, arsenic and cobalt beer-drinkers' disease, cardiovascular beri-beri, systemic hypertension, cardiac arrhythmias, stroke, atherosclerotic coronary heart disease (CHD), total mortality, and definitions of safe drinking limits. The basic disparity underlying all alcohol-health relations is between effects of lighter and heavier drinking.
Three decades of research shows that drinking small to moderate amounts of alcohol has cardiovascular benefits. A thorny issue for physicians is whether to recommend drinking to some patients
Observational studies suggest that heavy alcohol consumption may increase the risk of stroke while moderate consumption may decrease the risk.
To examine the association between alcohol consumption and relative risk of stroke.
Studies published in English-language journals were retrieved by searching MEDLINE (1966-April 2002) using Medical Subject Headings alcohol drinking, ethanol, cerebrovascular accident, cerebrovascular disorders, and intracranial embolism and thrombosis and the key word stroke; Dissertation Abstracts Online using the keywords stroke and alcohol; and bibliographies of retrieved articles.
From 122 relevant retrieved reports, 35 observational studies (cohort or case control) in which total stroke, ischemic stroke, or hemorrhagic (intracerebral or total) stroke was an end point; the relative risk or relative odds and their variance (or data to calculate them) of stroke associated with alcohol consumption were reported; alcohol consumption was quantified; and abstainers served as the reference group.
Information on study design, participant characteristics, level of alcohol consumption, stroke outcome, control for potential confounding factors, and risk estimates was abstracted independently by 3 investigators using a standardized protocol.
A random-effects model and meta-regression analysis were used to pool data from individual studies. Compared with abstainers, consumption of more than 60 g of alcohol per day was associated with an increased relative risk of total stroke, 1.64 (95% confidence interval [CI], 1.39-1.93); ischemic stroke, 1.69 (95% CI, 1.34-2.15); and hemorrhagic stroke, 2.18 (95% CI, 1.48-3.20), while consumption of less than 12 g/d was associated with a reduced relative risk of total stroke, 0.83 (95%, CI, 0.75-0.91) and ischemic stroke, 0.80 (95% CI, 0.67-0.96), and consumption of 12 to 24 g/d was associated with a reduced relative risk of ischemic stroke, 0.72 (95%, CI, 0.57-0.91). The meta-regression analysis revealed a significant nonlinear relationship between alcohol consumption and total and ischemic stroke and a linear relationship between alcohol consumption and hemorrhagic stroke.
These results indicate that heavy alcohol consumption increases the relative risk of stroke while light or moderate alcohol consumption may be protective against total and ischemic stroke.
Substantial evidence has shown that moderate drinkers have lower rates of coronary heart disease (CHD) than abstainers, but the effects of alcohol consumption among patients with established CHD are less clear. Alcohol intake has important effects on risk factors for reinfarction, including higher levels of high-density lipoprotein cholesterol and triglycerides, lower levels of fibrinogen and other prothrombotic factors, lower fibrinolytic potential, and antiplatelet activity. Studies of patients at risk for CHD, such as those with diabetes, hypertension, and hyperlipidemia, have shown that the association of moderate drinking and CHD is at least as strong as it is in the general population. Most recently, studies have found that survivors of acute myocardial infarction who drink moderately have a risk of death approximately 20%-30% lower than do abstainers or rare drinkers. Nonetheless, the risks and benefits of alcohol use remain complex, even among patients with CHD, and no simple recommendation regarding alcohol consumption can be made for all patients.