Supplementation With Low Doses of Vitamin E Protects LDL From Lipid Peroxidation in Men and Women

Gaubius Laboratory, TNO-PG, Leiden, The Netherlands.
Arteriosclerosis Thrombosis and Vascular Biology (Impact Factor: 6). 03/1995; 15(3):325-33. DOI: 10.1161/01.ATV.15.3.325
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There is accumulating evidence that oxidative modification of LDL is an important step in the process of atherogenesis and that antioxidants may protect LDL from oxidation. We and others have previously shown that ingestion of pharmacological doses of the antioxidant D,L-alpha-tocopherol (vitamin E), far above the recommended daily intake (ie, 12 to 15 IU/d for adults), increases the oxidation resistance of LDL. In this study, we ascertained the minimal supplementary dose of vitamin E necessary to protect LDL against oxidation in vitro. Twenty healthy volunteers (10 men and 10 women, aged 21 to 31 years) ingested consecutively 25, 50, 100, 200, 400, and 800 IU/d, D,L-alpha-tocopherol acetate during six 2-week periods. No changes were observed in LDL triglyceride content, fatty acid composition of LDL, or LDL size during the intervention. Concentrations of alpha-tocopherol in plasma and LDL were both 1.2 times the baseline values after the first period (25 IU/d) and 2.6 and 2.2 times, respectively, after the last period (800 IU/d). There was a linear increase in LDL alpha-tocopherol levels up to an intake of 800 IU/d (r = .79, P < .0001) and a good correlation between alpha-tocopherol in plasma and LDL (r = .66, P < .0001). Simultaneously, the resistance of LDL to oxidation was elevated dose-dependently (+28% after the last period) and differed significantly from the baseline resistance time even after ingestion of only 25 IU/d.(ABSTRACT TRUNCATED AT 250 WORDS)

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Available from: Hans M.G. Princen, Jul 14, 2014
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    • "There is increasing evidence that oxidative modification of low density lipoprotein (LDL) plays a key role in the development of atherosclerosis (Esterbauer et al, 1991; Princen et al, 1995; Nicolaı¨ew et al, 1998; O&apos;Byrne et al, 1998) and the effect of dietary fatty acids and antioxidants on the resistance of lipoprotein to oxidation is well known. A lower incidence of coronary heart disease (CHD) in Mediterranean countries has been correlated with a diet rich in fruit, vegetables, legumes and grains. "
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    ABSTRACT: To measure the incorporation of oleic acid and antioxidants (phenols and vitamin E) to low density lipoprotein (LDL) after acute and short-term ingestion of virgin olive oil. To study whether this incorporation contributes to an increase in LDL resistance to oxidation. Department of Food and Nutrition, University of Barcelona, Spain and Department of Lipids and Cardiovascular Epidemiology, IMIM, Barcelona, Spain. Sixteen healthy volunteers aged 25-65 y. To observe the change in the fatty acid profile, vitamin E, phenolic compounds and LDL oxidation-related variables after the postprandial phase and after daily ingestion of olive oil for one week. Few changes were observed in the postprandial phase. However, after a week of olive oil consumption there was an increase in oleic acid (P=0.015), vitamin E (P=0.047), phenolics (P=0.021) and lag time (P=0.000), and a decrease in the maximum amount of dienes (P=0.045) and oxidation rate (P=0.05). After ingestion of virgin olive oil, an increase in antioxidants and oleic acid in LDL was observed as well as an improvement of LDL resistance to oxidation. Our results support the idea that daily ingestion of virgin olive oil could protect LDL from oxidation. This study was supported by a research grant from Spain (ALI 97-1607-C02-02).
    European Journal of Clinical Nutrition 03/2002; 56(2):114-20. DOI:10.1038/sj.ejcn.1601293 · 2.71 Impact Factor
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    • "The potential antiatherogenic role of vitamin E emerged from experimental studies providing consistent evidence for the protective role of vitamin E not only in preventing the oxidation of low-density lipoproteins (LDL) [6] [7], but also in preventing a number of cellular events involved in the development of atherosclerosis as reviewed by several authors [8] [9] [10]. In particular, vitamin E limits the formation of foam cells in maintaining the capacity of LDL to be recognized by LDL receptors [11] and in decreasing the expression of scavenger receptors on macrophages [12] [13]. "
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    ABSTRACT: Epidemiological data regarding the preventive role of vitamin E in the pathogenesis of atherosclerosis have yielded conflicting results, possibly because endpoints considered were clinical events but not detection of atherosclerosis per se. Otherwise, it has been suggested that the measure of the erythrocyte α-tocopherol level may be more suitable to assess the human tocopherol status than its plasma level. We investigated the association between early atherosclerosis in superficial arteries assessed noninvasively and the α-tocopherol status in 261 asymptomatic men at risk for cardiovascular disease. α-Tocopherol concentrations in plasma, HDL, and erythrocytes were determined using a reverse-phase HPLC method. Detection of carotid plaques and measure of carotid intima–media thickness (IMT) were performed using high-resolution B-mode ultrasonography. The main result of this study is the observation of a negative correlation (P<0.01) between carotid IMT and erythrocyte α-tocopherol concentration, independently of conventional cardiovascular risk factors, whereas no such association has been found with plasma (total or HDL) α-tocopherol concentrations. No association has been evidenced between α-tocopherol concentrations and carotid plaques. These results emphasize the primary protective role of vitamin E in the early phases of atherosclerosis and the significance of the erythrocyte α-tocopherol concentration as a marker of atherosclerosis.
    Atherosclerosis 11/2001; 159(1-159):193-200. DOI:10.1016/S0021-9150(01)00493-2 · 3.99 Impact Factor
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    • "Vitamin E is the most important lipid-soluble antioxidant in the body (Princen et al, 1995; Jialal et al, 1995). In one dose ± response study Princen et al suggested that intake of 25 mgaday of vitamin E for 2 weeks was suf®cient to reduce the susceptibility of LDL to oxidation (Princen et al,1995). In another dose ± response study, Jialal et al investigated the effects of vitamin E intake in doses of 60, 200, 400, 800 and 1200 mgaday. "
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    ABSTRACT: We studied whether consumption of phenol-rich extra virgin olive oil affects the susceptibility of low density lipoproteins (LDL) to oxidation and other markers of oxidation in humans. Randomized cross-over intervention trial, stratified according to sex, age and energy intake. Division of Human Nutrition and Epidemiology, Wageningen University, The Netherlands. Forty-six healthy men and women completed the study. Subjects consumed two diets supplying 69 g per day of extra virgin olive oil either rich or poor in phenols for 3 weeks each. The mean difference in phenol intake between the treatments was 18 mg per day. Vitamin E intake was low during the whole study. Fasting blood samples were taken twice at the end of each period. Resistance of LDL and high density lipoprotein (HDL) to oxidation was not affected by treatment. The mean lag time of copper-induced formation of conjugated dienes was 1.6 min shorter in LDL and 0.4 min longer in HDL after the high phenol diet. Other markers of antioxidant capacity in plasma were also not affected: mean lipid hydroperoxides were 0.07 micromol/l higher, mean malondialdehydes were 0.001 micromol/l higher, mean protein carbonyls were 0.001 nmol/mg protein lower, and the mean ferric reducing ability of plasma (FRAP) was 0.006 mmol/l higher after the high phenol diet. All 95% confidence intervals enclosed zero. Serum cholesterol concentrations were not affected by the treatment. Consumption of 18 mg per day of phenols from extra virgin olive oil for 3 weeks did not affect LDL or HDL oxidation or other markers of antioxidant capacity in fasting plasma samples.
    European Journal of Clinical Nutrition 06/2001; 55(5):334-41. DOI:10.1038/sj.ejcn.1601161 · 2.71 Impact Factor
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