Antioxidants are everywhere – why not use them to save our lives?
Antioxidants protect the body from damage caused by harmful molecules called free radicals. Many experts believe this damage is a factor in the development of blood vessel disease (atherosclerosis), cancer, and other conditions. Damage to the heart and blood vessels is collectively known as cardiovascular disease and people with diabetes have a higher chance of developing it. Antioxidants are capable of stabilizing, or deactivating, free radicals before they attack cells. Antioxidants can save lives for people who have diabetes with cardiovascular disease.
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Given the role of oxidative damage in the development of CVD, antioxidant therapy seemed the obvious thing to try. It was therefore surprising that several large-scale clinical trials of patients with cardiovascular disease failed to show any benefit from antioxidant supplementation (2). There were indications, however, that a subset of patients in these trials might have derived a benefit from taking antioxidants. These patients had two things in common, namely diabetes and a particular form of the haptoglobin protein (3,4).
That this type of patient indeed benefits from antioxidant therapy has now been confirmed in a clinical trial (5). 1,434 diabetics with haptoglobin phenotype Hp 2-2 were randomly assigned to receive either 400 IU per day of vitamin E or placebo. After eighteen months the vitamin E group had less than half the number of heart attacks, strokes or cardiovascular deaths as the placebo group (2.2% vs 4.7%). These results were significant enough to halt the trial.
Since it is the primary role of haptoglobin to bind free hemoglobin and remove it from circulation, free hemoglobin and the oxidative damage it can cause had to be the critical factors.
When an atherosclerotic plaque breaks, red blood cells penetrate the arterial wall. This risk is magnified in diabetes due to more rapid red blood cell turnover and increased damage to the blood vessel wall. The red blood cells entering the arterial wall break down and release their hemoglobin, which ultimately generates free iron. Divalent iron can cause the generation of hydroxyl radicals and lipid peroxidation, especially the peroxidation of polyunsaturated fatty acids. It is the role of haptoglobin to bind the free hemoglobin for removal by macrophages, before peroxidation can damage the lipoproteins and their contents. The effectiveness with which haptoglobin can do this depends on its structure.
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