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Antioxidants are micronutrients that form compounds with so-called free radicals before these radicals can change or even destroy important structures in the body. Free radicals can be caused by ozone pollution, UV radiation, environmental toxins, nicotine, and pharmaceuticals, but a certain amount of exposure to free radicals is considered normal. However, if there is an excess of free radicals, so-called oxidative stress occurs. To prevent this, an optimal antioxidative status is necessary. People who are often exposed to stress, smoke, fly often or sunbathe, drink alcohol and are confronted with environmental pollution are advised to provide nutritional-physiological support for the body's antioxidant protective systems. A combination of different antioxidants proves to be more useful than a unilateral high dosage of individual substances, as the antioxidant vital substances support each other in their effect and recycle after consumption. 



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The body is constantly confronted with so-called free radicals, which not only form inside the body but also have an increased influence on the organism itself. Because these aggressive compounds are very reactive, they harm almost all structures of the human organism and trigger chain reactions, which lead to the formation of new radicals. Thus, free radicals are created during inflammatory processes, detoxification processes, physical activity, but also by external factors such as chemicals, radiation, acute and chronic stress as well as environmental and drug exposure. Also, the formation of free radicals is occasionally a desirable and important process. For example, immune cells produce specific free radicals to combat viruses and bacteria. However, when radical formation becomes rampant, one speaks of oxidative stress, which is a burden on the body and a major factor in the development of degenerative diseases, including rheumatic and neurodegenerative diseases, cancer, arteriosclerosis or diabetes, and cataracts.


To counter oxidative stress, the organism has enzymatic and non-enzymatic antioxidant systems that serve to balance the excess of free radicals. This property is called "antioxidant" because it prevents the biochemical process of oxidation. For these particular systems to function optimally, they are dependent on trigger substances from nutrition. Thus, plants with their constituents make a considerable contribution to improving the antioxidative status and to the protection of the organism. These food components act as so-called antioxidants and show a protective effect against numerous diseases according to studies and can, therefore, be used as a targeted accompanying measure in therapy and prevention. As so-called antioxidants, certain micronutrients such as vitamin C, vitamin E, minerals such as selenium and secondary plant substances can help to maintain an oxidative balance and protect the cells from oxidative stress. Vitamin E is regarded as the most important fat-soluble antioxidant in the human organism and provides a high protective factor to the cells, neutralizes aggressive oxygen radicals and can protect the cell walls and other body structures from damage. But vitamin E does not work alone. Together with vitamin C and other antioxidant components, it forms a protective system, so that this team of antioxidants supports each other in their effect. Vitamin C protects the cells from oxidative damage caused by free radicals, recycles oxidatively consumed vitamin E and is involved in the regeneration of glutathione. As a component of glutathione peroxidase, selenium performs an important antioxidant function and protects DNA, membranes, and erythrocytes from oxidative damage. Carotenoids also play an important role as radical scavengers by "defusing" free radicals and thus acting to protect and prevent radical-associated diseases, especially of the skin and eye. Secondary plant substances such as anthocyanins not only ensure the bright colors in food, they also play an important role in protecting against oxidative stress.


Studies have repeatedly highlighted the importance of enough antioxidant supply to protect the arteries, where especially vitamin C, vitamin E, and beta-carotene seem to play a particularly important role in this context. Furthermore, a suboptimal supply of antioxidants seems to be associated with cancer, highlighting the importance of antioxidative micronutrients in the development of this disease. The income of vitamin C, vitamin E, and alpha-lipoic acid can contribute to the protection from late diabetic damage. A further connection can be made between oxidative stress and neurodegenerative illnesses, with a protective effect of vitamin E together with vitamin C and with the emergence as well as the process of these disease patterns. A sufficient supply of antioxidants is also recommended in sports, where an increased occurrence of free radicals is observed. There the antioxidative effect of micronutrients can contribute to the avoidance of development restrictions as well as to the prevention of serious damages. In addition, people are exposed to increased oxidative stress due to environmental factors such as UV, ozone or pollution, but smokers and people with chronic use of medications such as paracetamol or cytostatic drugs also have a higher need for antioxidants. In the laboratory, exposure to free radicals can be determined by testing serum antioxidant capacity. A mean value of 305 µmol/l is considered the desired mean value. Individuals with values below this mean value can be regarded as undersupplied with antioxidants. Regular monitoring of the antioxidative status is suitable for individuals with chronic diseases or those caused by radicals as well as for monitoring the progress of antioxidative therapy. For individuals who are under an increased radical load, nutritional physiological support of the body's antioxidative protective systems is advisable. Since antioxidants support each other in their effect and recycle after consumption, a combination of different antioxidative effective vital substances is more sensible than a one-sided high dosage of an individual.


Antioxidants are used in the following areas of application:

  • To maintain a balanced antioxidant status during increased oxidative exposure to UV radiation, physical activity, physical and psychological stress.
  • In case of increased oxidative stress caused by chronic medication, tobacco and/or alcohol as well as by environmental pollution.
  • Therapeutic accompaniment for acute and chronic diseases to strengthen the antioxidative systems
  • To maintain the antioxidative bond in case of increased radical exposure, e.g. through smoking or frequent alcohol consumption.



Mild gastrointestinal disorders (flatulence, diarrhea) can occur when high doses of vitamin C are taken. An increased intake of vitamin E in patients who are already taking anticoagulant drugs can lead to a disorder in their ability to coagulate, as vitamin E has an antithrombotic effect. In persons with coagulation disorders and before surgery, the prolongation of the bleeding time must be considered. Higher dosages of vitamin E should always be combined with an appropriate amount of vitamin C. Vitamin E acts as a radical scavenger by releasing electrons and becoming a radical itself. Vitamin C recycles vitamin E radicals. High doses (over 800 mg or 1200 I.U.) can cause gastrointestinal complaints (diarrhea, flatulence, nausea). This can also happen when taking high doses of vitamin C (<500 mg). With selenium, chronic overdose can lead to neuropathies, hair loss, and brittle nails. Acute overdose of selenium can cause nausea, diarrhea and a garlicky breath odor. Beta-carotene in high doses can lead to a harmless yellowing of the skin in the long-term (> 3 weeks, > 30 mg/d).


NSAIDs (especially salicylates) inhibit the active transport of vitamin C through the intestinal wall. ASAIDs can lower vitamin C levels in the blood and white blood cells. Vitamin C administration protects against NSAID-induced mucous membrane damage. Corticosteroids lead to increased renal excretion and oxidation of vitamin C. When taking oral contraceptives, estrogens can increase the vitamin C requirement. When taking antiparkinson drugs (L-dopa), vitamin C can improve the absorption of L-dopa. In the case of nitrates, vitamin C reduces nitrate tolerance. High doses of vitamin E can increase the blood-thinning effect of ASA. Vitamin E can improve the tolerance of haloperidol (neuroleptics). Selenium enhances the antioxidant effect of vitamin E. vitamin E can counteract the prooxidative activity of iron. High vitamin E doses reduce the absorption of vitamin A and may inhibit the effect of vitamin K. Vitamin C regenerates oxidatively depleted vitamin E. High doses of omega-3 fatty acids can cause a drop in vitamin E levels. Neuroleptics increase the selenium requirement. Selenium can reduce the nephrotoxicity, cardiotoxicity, and neurotoxicity of cytostatic drugs. Selenium can reduce the need for corticosteroids (e.g. methylprednisolone, dexamethasone, prednisolone). Selenium improves the effect of thyroid preparations and binds heavy metals. Estrogenic medroxyprogesterone can change beta-carotene and vitamin A levels. Vitamin A deficiency is associated with an increased risk of worm infections. Taking vitamin A or beta-carotene improves the therapy of anthelmintics.


It is not recommended to take vitamin C for iron storage disease (hemochromatosis) and renal insufficiency, and vitamin C in high doses (<500 mg) if oxalate stones (urolithiasis) or hyperoxaluria are present. Carotenoids should not be taken for existing liver damage or renal insufficiency


Depending on the antioxidant, the groups of people and the field of application, different reference values apply for the supply.


1) Bieger, W.P., Neuner A. 2006. Die Pathophysiologie von Oxidativem Stress. Zs F Orthomol. Med. 3:6-12
2) Friedrichsen, H.P. 2006. Antioxidative Therapie. Zs F Orthomol Med. 29-30.
3) Bjelakovic, G. et al. 2012. Antioxidant supplements for prevention of mortality in healthy participants and patients with various diseases. Cochrane Database Syst Rev 14.
4) Gröber, U. 2006. Arzneimitteleinnahme und oxidativer Stress. Zs F Orthomol Med. 27-28.
5) Stargrove, M. B. et al. Herb, Nutrient, and Drug Interactions: Clinical Implications and Therapeutic Strategies, 1. Auflage. St. Louis, Missouri: Elsevier Health Sciences, 2008.

* These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.