There is a well known problem with antioxidants: It has not been proven that they prevent atherosclerosis or cancer.
This is strange because there is almost full agreement that the free radicals that antioxidants combat are the primary reasons for these killer illnesses. Whey then is the reputation of antioxidants not better?
There are many explanations. One is that they have had bad press. They work, but some say that swindlers manipulate the numbers and claim that the opposite. This is not without reason. A few years ago a Danish researcher, to his displeasure, had to announce that antioxidants reduce the risk of cancer by about 10%. This was apparently not statistically certain, but the annoyance of this announcement was so great that he simply had to say just the opposite. He declared confidently on television that they had it was discovered that antioxidants “simply accelerate cancer cells.” They understood them to be pure poison.
Did he really say that? Yes! But less gross manipulation also occurs. A favourite method is to, for example, ignore positive results. In the Danish Fitness and Nutrition Council’s latest report about antioxidants describes the unique French SU.VI.MAX study which showed that supplements of antioxidants decrease death rates by over a third. Despite this exceptional result, it is not described in the report’s conclusion. What is hidden is forgotten.
If SU.VI.MAX is unique it is because it is the only large long term randomised study where a broad array of antioxidants were used (vitamins C and E, selenium, beta-carotene, and zinc) instead of just one or two. Thereby we can dare to believe that free radicals are really being attacked. Large amounts of a single antioxidant can have the opposite effect, which is to say an increase in the amount of free radicals.
Consider atherosclerosis. It is widely believed that atherosclerosis is roughly due to the oxidation of LDL cholesterol by free radicals and the subsequent calcification which it causes. Therefore it should logically be possible to prevent it by neutralising the free radicals. Notice what the theory is stating: If the free radicals are neutralised, then atherosclerosis is prevented.
The wrong studies
Unfortunate this is not what has been studied! It seems that atherosclerosis has been studied, but not whether there are fewer free radicals when antioxidants are used and therefore whether the correct treatment was used. If the atherosclerosis became less pronounced, it was impossible to know whether it was for this reason. For example, a study was done with vitamin E without measuring free radicals. Often measurements on whether or not the vitamin was taken up by the intestines were not done. This is a necessary prerequisite for their effectiveness. When this was measured, the increased concentration in the blood was often insignificant.
But do supplements of vitamin E always neutralise free radicals? Not necessarily. It is probably wisest to combine with other antioxidants (vitamin C, selenium, etc.). In a study where participants were given 2,000 mg vitamin E, far more than what is found in a dietary supplement, no neutralisation was found.
Under any medicinal treatment controls are undertaken to see if the medicine does what it should. For example, when diabetics receive insulin it is known that it should diffuse into the tissues. This should cause a fall in blood sugar, which is, of course, measured as a control. But this type of banal measurement is lacking in clinical studies which antioxidants. Participants are not examined beforehand to see if they are strained by free radicals or if they are less strained after treatment. It is like giving someone insulin without knowing if he has diabetes or if his blood sugar falls as a result.
Why is this not measured? It is not due to ill will, there has been a lack of good methods of measurement. We now have them to a greater degree.
As mentioned, free radicals oxidise LDL cholesterol. A group of researchers from Cleveland have found that two of the oxidation products are extremely good markers for atherosclerosis in the coronary arteries: 9-HETE and F2-isoprostan. Dependent on the amount of these substances in the blood, two people of the same age, sex, blood pressure, smoking habits, and cholesterol have widely differing likelihoods for extreme atherosclerosis in the coronary arteries. If one is in the highest fourth of the population with regards to F2-isoprostan concentration while the other is in the lowest fourth, then the first’s risk is ten times greater than the second’s. This is a gigantic difference.
A more reasonable study on antioxidants should include the following:
A large array of antioxidants should be taken, not just a single antioxidant.
Participants must have elevated levels of, for example, F2-isoprostan. Otherwise the degree of need for antioxidants is unknown.
It should be measured whether the amount of, for example, F2-isoprostan (which is an expression for free radical levels) falls under treatment. Otherwise the study is without merit.
None of these things has yet been done. The clinical research of antioxidants still uses training wheels!
References:
- Shishehbor MH et al. Systemic elevations of free radical oxidation products of arachidonic acid are associated with angiographic evidence of coronary artery disease. Free Radical Biology & Medicine 2006;41:1678-83.
- Hercberg S et al. The SU.VI.Max study. Arch Int Med 2004;164:2335-2342
- Meagher E et al. Effects of vitamin E on lipid peroxidation in healthy persons. JAMA 2001;285:1178-82.
Niels Hertz
