Alpha-Tocopherol Supplementation in Healthy Individuals Reduces Low-Density Lipoprotein Oxidation but Not Atherosclerosis The Vitamin E Atherosclerosis Prevention Study (VEAPS)
Background— Epidemiological studies have demonstrated an inverse relationship between vitamin E intake and cardiovascular disease (CVD) risk. In contrast, randomized controlled trials have reported conflicting results as to whether vitamin E supplementation reduces atherosclerosis progression and CV...
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Published in | Circulation (New York, N.Y.) Vol. 106; no. 12; pp. 1453 - 1459 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Hagerstown, MD
Lippincott Williams & Wilkins
17.09.2002
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Subjects | |
Online Access | Get full text |
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Abstract | Background—
Epidemiological studies have demonstrated an inverse relationship between vitamin E intake and cardiovascular disease (CVD) risk. In contrast, randomized controlled trials have reported conflicting results as to whether vitamin E supplementation reduces atherosclerosis progression and CVD events.
Methods and Results—
The study population consisted of men and women ≥40 years old with an LDL cholesterol level ≥3.37 mmol/L (130 mg/dL) and no clinical signs or symptoms of CVD. Eligible participants were randomized to DL-α-tocopherol 400 IU per day or placebo and followed every 3 months for an average of 3 years. The primary trial end point was the rate of change in the common carotid artery far-wall intima-media thickness (IMT) assessed by computer image-processed B-mode ultrasonograms. A mixed effects model using all determinations of IMT was used to test the hypothesis of treatment differences in IMT change rates. Compared with placebo, α-tocopherol supplementation significantly raised plasma vitamin E levels (
P
<0.0001), reduced circulating oxidized LDL (
P
=0.03), and reduced LDL oxidative susceptibility (
P
<0.01). However, vitamin E supplementation did not reduce the progression of IMT over a 3-year period compared with subjects randomized to placebo.
Conclusions—
The results are consistent with previous randomized controlled trials and extend the null results of vitamin E supplementation to the progression of IMT in healthy men and women at low risk for CVD. |
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AbstractList | Epidemiological studies have demonstrated an inverse relationship between vitamin E intake and cardiovascular disease (CVD) risk. In contrast, randomized controlled trials have reported conflicting results as to whether vitamin E supplementation reduces atherosclerosis progression and CVD events.BACKGROUNDEpidemiological studies have demonstrated an inverse relationship between vitamin E intake and cardiovascular disease (CVD) risk. In contrast, randomized controlled trials have reported conflicting results as to whether vitamin E supplementation reduces atherosclerosis progression and CVD events.The study population consisted of men and women > or =40 years old with an LDL cholesterol level > or =3.37 mmol/L (130 mg/dL) and no clinical signs or symptoms of CVD. Eligible participants were randomized to DL-alpha-tocopherol 400 IU per day or placebo and followed every 3 months for an average of 3 years. The primary trial end point was the rate of change in the common carotid artery far-wall intima-media thickness (IMT) assessed by computer image-processed B-mode ultrasonograms. A mixed effects model using all determinations of IMT was used to test the hypothesis of treatment differences in IMT change rates. Compared with placebo, alpha-tocopherol supplementation significantly raised plasma vitamin E levels (P<0.0001), reduced circulating oxidized LDL (P=0.03), and reduced LDL oxidative susceptibility (P<0.01). However, vitamin E supplementation did not reduce the progression of IMT over a 3-year period compared with subjects randomized to placebo.METHODS AND RESULTSThe study population consisted of men and women > or =40 years old with an LDL cholesterol level > or =3.37 mmol/L (130 mg/dL) and no clinical signs or symptoms of CVD. Eligible participants were randomized to DL-alpha-tocopherol 400 IU per day or placebo and followed every 3 months for an average of 3 years. The primary trial end point was the rate of change in the common carotid artery far-wall intima-media thickness (IMT) assessed by computer image-processed B-mode ultrasonograms. A mixed effects model using all determinations of IMT was used to test the hypothesis of treatment differences in IMT change rates. Compared with placebo, alpha-tocopherol supplementation significantly raised plasma vitamin E levels (P<0.0001), reduced circulating oxidized LDL (P=0.03), and reduced LDL oxidative susceptibility (P<0.01). However, vitamin E supplementation did not reduce the progression of IMT over a 3-year period compared with subjects randomized to placebo.The results are consistent with previous randomized controlled trials and extend the null results of vitamin E supplementation to the progression of IMT in healthy men and women at low risk for CVD.CONCLUSIONSThe results are consistent with previous randomized controlled trials and extend the null results of vitamin E supplementation to the progression of IMT in healthy men and women at low risk for CVD. Epidemiological studies have demonstrated an inverse relationship between vitamin E intake and cardiovascular disease (CVD) risk. In contrast, randomized controlled trials have reported conflicting results as to whether vitamin E supplementation reduces atherosclerosis progression and CVD events. The study population consisted of men and women > or =40 years old with an LDL cholesterol level > or =3.37 mmol/L (130 mg/dL) and no clinical signs or symptoms of CVD. Eligible participants were randomized to DL-alpha-tocopherol 400 IU per day or placebo and followed every 3 months for an average of 3 years. The primary trial end point was the rate of change in the common carotid artery far-wall intima-media thickness (IMT) assessed by computer image-processed B-mode ultrasonograms. A mixed effects model using all determinations of IMT was used to test the hypothesis of treatment differences in IMT change rates. Compared with placebo, alpha-tocopherol supplementation significantly raised plasma vitamin E levels (P<0.0001), reduced circulating oxidized LDL (P=0.03), and reduced LDL oxidative susceptibility (P<0.01). However, vitamin E supplementation did not reduce the progression of IMT over a 3-year period compared with subjects randomized to placebo. The results are consistent with previous randomized controlled trials and extend the null results of vitamin E supplementation to the progression of IMT in healthy men and women at low risk for CVD. Background— Epidemiological studies have demonstrated an inverse relationship between vitamin E intake and cardiovascular disease (CVD) risk. In contrast, randomized controlled trials have reported conflicting results as to whether vitamin E supplementation reduces atherosclerosis progression and CVD events. Methods and Results— The study population consisted of men and women ≥40 years old with an LDL cholesterol level ≥3.37 mmol/L (130 mg/dL) and no clinical signs or symptoms of CVD. Eligible participants were randomized to DL-α-tocopherol 400 IU per day or placebo and followed every 3 months for an average of 3 years. The primary trial end point was the rate of change in the common carotid artery far-wall intima-media thickness (IMT) assessed by computer image-processed B-mode ultrasonograms. A mixed effects model using all determinations of IMT was used to test the hypothesis of treatment differences in IMT change rates. Compared with placebo, α-tocopherol supplementation significantly raised plasma vitamin E levels ( P <0.0001), reduced circulating oxidized LDL ( P =0.03), and reduced LDL oxidative susceptibility ( P <0.01). However, vitamin E supplementation did not reduce the progression of IMT over a 3-year period compared with subjects randomized to placebo. Conclusions— The results are consistent with previous randomized controlled trials and extend the null results of vitamin E supplementation to the progression of IMT in healthy men and women at low risk for CVD. |
Author | Liu, Ci-hua Selzer, Robert H. LaBree, Laurie Mack, Wendy J. Liu, Chao-ran Hwang, Juliana Mahrer, Peter R. Hodis, Howard N. Azen, Stanley P. Sevanian, Alex |
Author_xml | – sequence: 1 givenname: Howard N. surname: Hodis fullname: Hodis, Howard N. organization: From the Departments of Medicine (H.N.H.) and Preventive Medicine (H.N.H., W.J.M., L.L., S.P.A.) and the Atherosclerosis Research Unit (H.N.H., W.J.M., L.L., A.S., C.-r. Liu, C.-h. Liu, J.H., R.H.S., S.P.A.), University of Southern California Keck School of Medicine; Department of Molecular Pharmacology and Toxicology (H.N.H., A.S., J.H.), University of Southern California School of Pharmacy; and Kaiser Permanente Medical Center (P.R.M.), Los Angeles, Calif; and Jet Propulsion Laboratory, California – sequence: 2 givenname: Wendy J. surname: Mack fullname: Mack, Wendy J. organization: From the Departments of Medicine (H.N.H.) and Preventive Medicine (H.N.H., W.J.M., L.L., S.P.A.) and the Atherosclerosis Research Unit (H.N.H., W.J.M., L.L., A.S., C.-r. Liu, C.-h. Liu, J.H., R.H.S., S.P.A.), University of Southern California Keck School of Medicine; Department of Molecular Pharmacology and Toxicology (H.N.H., A.S., J.H.), University of Southern California School of Pharmacy; and Kaiser Permanente Medical Center (P.R.M.), Los Angeles, Calif; and Jet Propulsion Laboratory, California – sequence: 3 givenname: Laurie surname: LaBree fullname: LaBree, Laurie organization: From the Departments of Medicine (H.N.H.) and Preventive Medicine (H.N.H., W.J.M., L.L., S.P.A.) and the Atherosclerosis Research Unit (H.N.H., W.J.M., L.L., A.S., C.-r. Liu, C.-h. Liu, J.H., R.H.S., S.P.A.), University of Southern California Keck School of Medicine; Department of Molecular Pharmacology and Toxicology (H.N.H., A.S., J.H.), University of Southern California School of Pharmacy; and Kaiser Permanente Medical Center (P.R.M.), Los Angeles, Calif; and Jet Propulsion Laboratory, California – sequence: 4 givenname: Peter R. surname: Mahrer fullname: Mahrer, Peter R. organization: From the Departments of Medicine (H.N.H.) and Preventive Medicine (H.N.H., W.J.M., L.L., S.P.A.) and the Atherosclerosis Research Unit (H.N.H., W.J.M., L.L., A.S., C.-r. Liu, C.-h. Liu, J.H., R.H.S., S.P.A.), University of Southern California Keck School of Medicine; Department of Molecular Pharmacology and Toxicology (H.N.H., A.S., J.H.), University of Southern California School of Pharmacy; and Kaiser Permanente Medical Center (P.R.M.), Los Angeles, Calif; and Jet Propulsion Laboratory, California – sequence: 5 givenname: Alex surname: Sevanian fullname: Sevanian, Alex organization: From the Departments of Medicine (H.N.H.) and Preventive Medicine (H.N.H., W.J.M., L.L., S.P.A.) and the Atherosclerosis Research Unit (H.N.H., W.J.M., L.L., A.S., C.-r. Liu, C.-h. Liu, J.H., R.H.S., S.P.A.), University of Southern California Keck School of Medicine; Department of Molecular Pharmacology and Toxicology (H.N.H., A.S., J.H.), University of Southern California School of Pharmacy; and Kaiser Permanente Medical Center (P.R.M.), Los Angeles, Calif; and Jet Propulsion Laboratory, California – sequence: 6 givenname: Chao-ran surname: Liu fullname: Liu, Chao-ran organization: From the Departments of Medicine (H.N.H.) and Preventive Medicine (H.N.H., W.J.M., L.L., S.P.A.) and the Atherosclerosis Research Unit (H.N.H., W.J.M., L.L., A.S., C.-r. Liu, C.-h. Liu, J.H., R.H.S., S.P.A.), University of Southern California Keck School of Medicine; Department of Molecular Pharmacology and Toxicology (H.N.H., A.S., J.H.), University of Southern California School of Pharmacy; and Kaiser Permanente Medical Center (P.R.M.), Los Angeles, Calif; and Jet Propulsion Laboratory, California – sequence: 7 givenname: Ci-hua surname: Liu fullname: Liu, Ci-hua organization: From the Departments of Medicine (H.N.H.) and Preventive Medicine (H.N.H., W.J.M., L.L., S.P.A.) and the Atherosclerosis Research Unit (H.N.H., W.J.M., L.L., A.S., C.-r. Liu, C.-h. Liu, J.H., R.H.S., S.P.A.), University of Southern California Keck School of Medicine; Department of Molecular Pharmacology and Toxicology (H.N.H., A.S., J.H.), University of Southern California School of Pharmacy; and Kaiser Permanente Medical Center (P.R.M.), Los Angeles, Calif; and Jet Propulsion Laboratory, California – sequence: 8 givenname: Juliana surname: Hwang fullname: Hwang, Juliana organization: From the Departments of Medicine (H.N.H.) and Preventive Medicine (H.N.H., W.J.M., L.L., S.P.A.) and the Atherosclerosis Research Unit (H.N.H., W.J.M., L.L., A.S., C.-r. Liu, C.-h. Liu, J.H., R.H.S., S.P.A.), University of Southern California Keck School of Medicine; Department of Molecular Pharmacology and Toxicology (H.N.H., A.S., J.H.), University of Southern California School of Pharmacy; and Kaiser Permanente Medical Center (P.R.M.), Los Angeles, Calif; and Jet Propulsion Laboratory, California – sequence: 9 givenname: Robert H. surname: Selzer fullname: Selzer, Robert H. organization: From the Departments of Medicine (H.N.H.) and Preventive Medicine (H.N.H., W.J.M., L.L., S.P.A.) and the Atherosclerosis Research Unit (H.N.H., W.J.M., L.L., A.S., C.-r. Liu, C.-h. Liu, J.H., R.H.S., S.P.A.), University of Southern California Keck School of Medicine; Department of Molecular Pharmacology and Toxicology (H.N.H., A.S., J.H.), University of Southern California School of Pharmacy; and Kaiser Permanente Medical Center (P.R.M.), Los Angeles, Calif; and Jet Propulsion Laboratory, California – sequence: 10 givenname: Stanley P. surname: Azen fullname: Azen, Stanley P. organization: From the Departments of Medicine (H.N.H.) and Preventive Medicine (H.N.H., W.J.M., L.L., S.P.A.) and the Atherosclerosis Research Unit (H.N.H., W.J.M., L.L., A.S., C.-r. Liu, C.-h. Liu, J.H., R.H.S., S.P.A.), University of Southern California Keck School of Medicine; Department of Molecular Pharmacology and Toxicology (H.N.H., A.S., J.H.), University of Southern California School of Pharmacy; and Kaiser Permanente Medical Center (P.R.M.), Los Angeles, Calif; and Jet Propulsion Laboratory, California |
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Copyright | 2002 INIST-CNRS |
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CorporateAuthor | VEAPS Research Group |
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Keywords | Human Prognosis Cardiovascular disease Cholesterol LDL Controlled therapeutic trial E-Vitamins Antioxidant Vascular disease Lipoprotein LDL Chemotherapy Treatment Atherosclerosis Oxidation Tocopherol |
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Epidemiological studies have demonstrated an inverse relationship between vitamin E intake and cardiovascular disease (CVD) risk. In contrast,... Epidemiological studies have demonstrated an inverse relationship between vitamin E intake and cardiovascular disease (CVD) risk. In contrast, randomized... |
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SubjectTerms | Adult Aged alpha-Tocopherol - administration & dosage alpha-Tocopherol - therapeutic use Antioxidants - administration & dosage Antioxidants - therapeutic use Arteriosclerosis - blood Arteriosclerosis - diagnostic imaging Arteriosclerosis - prevention & control Biological and medical sciences Carotid Artery, Common - diagnostic imaging Dietary Supplements Disease Progression Female General and cellular metabolism. Vitamins Humans Lipoproteins, LDL - blood Male Medical sciences Middle Aged Patient Compliance Pharmacology. Drug treatments Tunica Intima - diagnostic imaging Tunica Media - diagnostic imaging Ultrasonography |
Subtitle | The Vitamin E Atherosclerosis Prevention Study (VEAPS) |
Title | Alpha-Tocopherol Supplementation in Healthy Individuals Reduces Low-Density Lipoprotein Oxidation but Not Atherosclerosis |
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