Relation Between Alcohol Consumption and C-Reactive Protein Levels in the Adult US Population

Scott H. Stewart, MD, MS, Arch G. Mainous III, PhD, Greg Gilbert, MSPH

Disclosures

J Am Board Fam Med. 2002;15(6) 

In This Article

Abstract and Introduction

Background: Moderate alcohol consumption has been linked to a decreased risk of cardiovascular death. Systemic inflammation as indicated by elevated levels of C-reactive protein might play a role in this relation.
Methods: To evaluate the association of alcohol consumption with C-reactive protein, we analyzed the findings of the Third National Health and Nutrition Examination, a population-based survey representing the noninstitutionalized US population. Participants were aged 17 and older (n = 11,572). The main outcome measures studied were probability of C-reactive protein measurements being greater than 0.30 mg/dL (corresponding to the 75th percentile for the population) stratified by categories of alcohol consumption. Multivariate logistic regression was used to adjust for potential confounders.
Results: Among nondrinkers 31% had elevated C-reactive protein levels, compared with 21% of low-to-moderate-frequency drinkers and 18% of high-frequency drinkers. In a model adjusted for confounding variables, those who drank 1 to 10 times per month (OR 0.83, 95% CI 0.72-0.95), 11 to 30 times (OR 0.74, 95% CI 0.62-0.88), and more than 60 times per month (OR 0.67, 95% CI 0.48-0.93) were less likely than nondrinkers to have elevated C-reactive protein levels.
Conclusions: Alcohol consumption is associated with a decreased probability of elevated C-reactive protein levels. This association supports an anti-inflammatory mechanism by which moderate alcohol use might protect against cardiovascular death.

Light to moderate consumption of ethanol has consistently been linked to a decrease in cardiovascular disease mortality, as reviewed elsewhere.[1] A protective effect of alcohol use on cardiovascular disease is suggested by the consistency of the epidemiologic evidence, as well as findings that show metabolizers of alcohol are more likely to experience a decrease in the incidence of myocardial infarction.[2] Additional evidence indicates that current drinkers who have a myocardial infarction have a better prognosis than alcohol abstainers.[3]

Clinicians are now faced with the increasingly challenging dilemma of deciding whether light to moderate alcohol use might be beneficial for patients at higher risk of coronary artery disease. Although most experts would not currently support recommending alcohol use to abstainers,[4] improved knowledge of the mechanisms by which alcohol protects against ischemic heart disease death is needed to aid in determining who is most and least likely to benefit from light drinking. Earlier studies suggest that increases in high-density lipoprotein (HDL)-cholesterol could account for approximately 50% of the protective effect of alcohol,[5,6] but it is clear that other factors are involved. If the beneficial effects of alcohol are mediated through established risk factors, epidemiologic studies should discern an association between alcohol use and the risk factors.

C-reactive protein is an acute phase reactant and marker of underlying systemic inflammation.[7] Circulating at low concentrations in healthy individuals, it rises dramatically in response to infection, inflammation, and injury. During the last decade, evidence has accumulated that an elevated level of C-reactive protein is an independent risk factor for myocardial infarction and peripheral vascular disease.[8,9] This understanding has paralleled the recognition of atherosclerosis as a systemic inflammatory disease.[10] Some epidemiologic evidence suggests that the protective effect of alcohol on ischemic heart disease death might be partially mediated through an anti-inflammatory action of alcohol.[11] We undertook this cross-sectional study to determine the association of alcohol use with C-reactive protein levels in a sample representative of the US population. Positive findings from this study would provide additional support for an anti-inflammatory effect of alcohol. Negative findings would suggest the need for reconsideration of the anti-inflammatory hypothesis and indicate that other potential mechanisms for the beneficial effects of light to moderate alcohol consumption need to be explored.

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