Abstract

P77 Background. In a previous report on antioxidant intake and 1.5 year progression of carotid intima-media thickness (IMT), we reported the unexpected finding that intake of vitamin C supplements was associated with increased IMT progression. The current paper extends those analyses to 3 years of follow-up. Methods. The cohort of 573 employed women and men was aged 40-60 years and free of CVD at entry. Common carotid IMT (by B-mode ultrasound), supplement intake (by questionnaire) and food intake (by 24-hr recalls) were measured over 3 examinations at 1.5 year intervals. IMT progression at the follow-ups (microns per year) was regressed on intake of antioxidants from different sources (average of baseline and 1.5 year follow-up) in a repeated measures model. Results. IMT progressed an average of 10.0 μm/yr (SD=16.5) among the 500 (87%) members of the cohort with follow-up. After adjustment for CVD risk factors, energy intake, and antioxidant intake from other sources, IMT progression (mean±SE) increased from 7.6±1.8 μm/yr among persons reporting no intake of vitamin C supplements to 20.3±2.6 μm/yr in the highest quartile of vitamin C supplement intake (≥857 mg/day)(p-trend=0.0005). In contrast, IMT progression declined from 10.2±1.4 μm/yr among persons reporting no intake of vitamin E supplements to 1.5±2.8 μm/yr among those in the highest quartile of vitamin E supplement intake (≥443 IU/day)(p-trend=0.02). Reduced progression was observed only in this top quartile of vitamin E supplement intake. Smaller reductions in IMT progression were also observed for high intake of vitamin C from food (indicative of a diet rich in fruits and vegetables) and intake of multiple vitamins (≥ 1 tablet/wk). Vitamin E from food was not associated with IMT progression. Conclusion. Vitamin C supplements may promote early atherosclerosis at higher doses, while vitamin E supplement intake above 450 IU/day may block early atherosclerotic progression. Our findings suggest that completed trials of vitamin E and CHD may have failed to detect benefits because of insufficient dose and intervention at later, rather than earlier, stages of disease.

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