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Alcohol Consumption and Plasma Concentration of CRP - Alcohol Consumption and Plasma Concentration of CRP
Description:
This study sought to determine the relationship between alcohol consumption and CRP
Study Design
Study Design:
Patients Enrolled: 2843
Mean Follow Up: 6 months
Female: 39
Patient Populations:
Enrollment in the PRINCE study. Enrollment criteria included US residents from physician community practices.
Exclusions:
Known chronic inflammatory conditions, need for anti-inflammatory therapy, use of statin therapy within the 6-month period prior to enrollment, and contraindications to statin therapy.
Drug/Procedures Used:
CRP levels were assessed at baseline. Self-reported alcohol consumption and other baseline variables were recorded. Alcohol consumption was grouped as no alcohol intake or <1 drink per month (group 1), 1-3 drinks per month (group 2), 1-4 drinks per week (group 3), 5-7 drinks per week (group 4), or >=2 drinks daily (group 5). CRP levels were also assessed at 6 months in patients in the pravastatin arm only.
Concomitant Medications:
Data were drawn from the Pravastatin Inflammation/CRP Evaluation (PRINCE) Study, a multicenter community-based trial of pravastatin or placebo on CRP levels at 6 month follow-up.
Principal Findings:
Nondrinkers (group 1) were more likely to be women (49.8% vs 13.1%, p<0.001) and to have diabetes (23.4% vs 6.9%, p<0.001) and less likely to be smokers (14.2% vs 26.2%, p<0.001) compared with heavier consumers of alcohol (group 5). CRP levels decreased as alcohol consumption increased until reaching the highest level of alcohol intake, where it remained level. Median CRP levels were 2.60 mg/L (interquartile range 1.20-5.30 mg/L), 2.20 mg/L (IQR 1.00-4.40 mg/L), 1.70 mg/L (IQR 0.80-3.80 mg/L), 1.60 mg/L (IQR 0.80-3.30 mg/L), and 1.80 mg/L (IQR 0.80-2.90 mg/L), for groups 1-5, respectively. Similar relationships occurred in subgroups of men, women not taking hormone replacement therapy (which has previously been shown to be related to CRP levels), nonsmokers, and patients with and without a history of cardiovascular disease (p<0.001 for each). The relation between CRP and alcohol consumption remained significant after adjustment for past and current smoking, systolic blood pressure, diabetes, BMI, HDL cholesterol, sex, and aspirin use (p<0.001 for trend). No correlation was observed between alcohol intake and change in CRP levels at 6 months in patients in the pravastatin arm who had 6 month CRP assessment (r=0.01, p=0.52).
Interpretation:
Among patients without a history of CVD, moderate alcohol intake was associated lower CRP levels compared with no or minimal alcohol consumption. Other studies such as the Physicians' Health Study and the Nurses' Health Study have shown an association between light to moderate alcohol intake and lower cardiovascular mortality compared with heavy or no alcohol intake. While the mechanism of action is not clearly established, data from the present trial suggest a possible role in the reduction of the inflammatory process may explain part of the reductions in cardiovascular mortality associated with moderate alcohol consumption. It should be noted that self-reported alcohol intake may underestimate the true consumption rate. Additionally, data on type of alcoholic beverages consumed was not ascertained in this study. Other studies have suggested a relation between the type of alcohol consumed and the cardioprotective effects of drinking.
References:
Circulation. 2003;107:443-447.
Keywords: Body Mass Index, Ethanol, Pravastatin, Coronary Disease, Blood Pressure, Cholesterol, HDL, Hormone Replacement Therapy, Diabetes Mellitus, Smoking
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