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Anti-oxidants-- a protective role in cardiovascular disease?
1Clinical Pharmacology Unit, The University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, UK. s.maxwell@ed.ac.uk
Insights
Antioxidant vitamins may not prevent cardiovascular disease (CVD) in humans, despite promising animal and observational studies. Clinical trials failed to show benefits, suggesting a need to re-evaluate their role in CVD prevention.
Area of Science:
- Nutritional biochemistry
- Cardiovascular disease research
- Oxidative stress mechanisms
Background:
- Established cardiovascular disease (CVD) risk factors like hypertension and diabetes don't explain all clinical events.
- Increased oxidative stress in blood vessels is implicated in CVD pathophysiology.
- Animal studies and epidemiological data suggest antioxidants may prevent CVD.
Purpose of the Study:
- To critically examine the evidence for antioxidant therapy in CVD prevention.
- To explore reasons for the discrepancy between preclinical/epidemiological data and clinical trial outcomes.
Main Methods:
- Review of animal model studies on antioxidant efficacy.
- Analysis of epidemiological studies correlating antioxidant intake/levels with CVD rates.
- Evaluation of results from large prospective randomized controlled trials of antioxidant interventions.
Main Results:
- Animal studies and some epidemiological data suggest a protective role for antioxidants against CVD.
- Intervention trials, particularly with vitamin E, have largely failed to demonstrate significant benefits in high-risk populations.
- Antioxidants showed benefits on surrogate markers like endothelial function and lipoprotein oxidation in some studies.
Conclusions:
- The hypothesis that antioxidant therapy prevents CVD in humans is not supported by current evidence from large-scale trials.
- Discrepancies between observational data and intervention trial results require further investigation.
- The role of antioxidants in CVD prevention remains uncertain and may be context-dependent.
Abstract:
Established risk factors for cardiovascular disease (CVD), such as hypertension, smoking and diabetes mellitus, explain only some of the observed variation in clinical events. This has maintained interest in other nutritional and biochemical factors that might contribute to the underlying pathophysiology of CVD. All of these risk factors are associated with increased oxidative stress in the vessel wall, which may contribute to CVD by several mechanisms. Studies in animal models of CVD have suggested that natural and synthetic anti-oxidants can prevent the development of clinical end points. These observations have generated the hypothesis that anti-oxidant therapy might also prevent CVD in human populations. This has been supported by epidemiological studies showing a negative correlation between circulating concentrations or dietary intake of natural anti-oxidant vitamins and CVD event rate. Many studies have also demonstrated a beneficial effect of anti-oxidants on surrogate markers of CVD such as endothelial function and lipoprotein oxidation. However, the results of large prospective randomised controlled intervention trials, mostly involving vitamin E in patients at increased risk of CVD, have been disappointing and have failed to demonstrate the anticipated benefits. This paper will critically examine the evidence and try to offer some explanation for the apparent failure of animal and epidemiological data to translate into meaningful clinical benefits.