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Alcohol consumption and atherosclerosis: what is the relation? Prospective results from the Bruneck Study
Insights
Regular alcohol consumption shows a dose-dependent effect on atherosclerosis. Light drinking may offer protection, while heavy drinking increases risk, impacting arterial disease progression.
Area of Science:
- Cardiovascular epidemiology
- Alcohol's impact on vascular health
- Atherosclerosis research
Background:
- The relationship between regular alcohol intake and atherogenesis remains debated.
- Prospective population-based studies are crucial for understanding alcohol's effects on atherosclerosis.
- The Bruneck Study addresses this gap by examining atherosclerosis risk factors.
Purpose of the Study:
- To investigate the association between alcohol consumption and the development of carotid atherosclerosis.
- To determine if alcohol intake influences early and advanced stages of atherogenesis.
- To explore potential mechanisms behind alcohol's effects on arterial disease.
Main Methods:
- Prospective population-based survey (Bruneck Study) with over 90% follow-up.
- High-resolution duplex ultrasonography to monitor changes in carotid atherosclerosis.
- Standardized questionnaires and diet records to quantify alcohol intake.
Main Results:
- Occasional alcohol intake showed no effect on atherogenesis.
- Light alcohol consumption (<50 g/d) was associated with a J-shaped reduced risk of early carotid atherosclerosis, potentially via LDL cholesterol inhibition.
- Heavy alcohol consumption (>=100 g/d) showed an excess risk of atherosclerosis, surpassing that of heavy smoking.
- A U-shaped association was observed for advanced carotid atherosclerosis (stenosis).
Conclusions:
- Alcohol's effects on arterial disease are dose-dependent, influencing atherogenesis progression.
- Light drinking may provide cardiovascular protection through antithrombotic effects and reduced LDL cholesterol impact.
- Findings highlight the complex, dual role of alcohol in cardiovascular health.
Background And Purpose:
Potential effects of regular alcohol consumption on atherogenesis are still controversial mainly due to the lack of prospective population-based studies.
Methods:
The Bruneck Study is a prospective population-based survey of atherosclerosis and its risk factors. The study population comprises a sex- and age-stratified random sample of men and women aged 40 to 79 years. Participation and follow-up were more than 90% complete. Changes in carotid atherosclerosis between the 1990 baseline and the first follow-up in 1995 were monitored by high-resolution duplex ultrasonography. Alcohol intake was quantified with a standardized questionnaire and prospective diet records.
Results:
Alcohol consumption less than once a week (occasional drinking) had no effect on atherogenesis. The association between regular alcohol intake and incident carotid atherosclerosis (early atherogenesis) was J-shaped, with light drinkers facing a lower risk than either heavy drinkers or abstainers. Protection offered by alcohol consumption of <50 g/d appeared to act through inhibition of the injurious action of high levels of low-density lipoprotein (LDL) cholesterol. Excess risk of incident atherosclerosis observed among heavy alcohol consumers (> or =100 g/d) clearly surpassed the risk burden afforded by heavy smoking. The association between regular alcohol intake and incident carotid stenosis (advanced atherogenesis) was U-shaped. Odds ratios were generally shifted toward protection and did not rely on LDL cholesterol levels. We failed to find any differential effects of alcohol from various sources. All associations remained independently significant when we adjusted for lifestyle, coincidental smoking, and the metabolic complex associated with drinking.
Conclusions:
Our findings support the view that adverse and beneficial effects of alcohol on arterial disease are mediated in part by a dose-dependent promotion or deceleration of atherogenesis. The protection afforded by light drinking may possibly be attributed to antithrombotic effects and inhibition of the atherogenic action of high levels of LDL cholesterol.