It is now recognised that many human pathologic conditions are associated with increased oxidation, mainly as a consequence of oxygenated free radicals. Free radical oxidation is a result of an oxidant material interacting with a biological constituent, such as a cell membrane lipid or a protein, to produce a free-radical species that can then cause a significant degeneration of these cells or tissues. Lipid peroxides, for example, are created by a series of oxidation reactions of unsaturated lipids and have been recognized as important degradation biomolecules involved in the aging process at a cellular level.
This oxidative stress from free radicals can affect the lipids in cell membranes by peroxidation, the nucleic acids by initiating carcinogenesis and proteins causing tissue damage. The flow on effect leads to chronic disease developing. These may include: arthritis and inflammatory diseases, atherosclerosis, stroke, autoimmune conditions, cancer, cataracts, contact dermatitis, coronary heart disease, drug toxicity, emphysema, accelerated aging, liver cirrhosis, multiple sclerosis, Parkinson’s disease, Alzheimer’s, neurologic degeneration, vascular disorders and lowered immunity in general.
Antioxidants are synthesized in the body, obtained from the diet or through supplementation. These antioxidants include enzymes such as superoxide dismutase (SOD), catalase, glutathione peroxidase, glutathione reductase, dehydroascorbate, reductase, and thioredoxin reductase. Hydrophilic (water loving) antioxidants such as ascorbate, urate and glutathione (GSH) and the hydrophobic (water fearing) antioxidants include tocopherols (Vit E), CO Q10, flavonoids and carotenoids.
The enzymes themselves, require many of the nutrient antioxidants to be able to exert their effects, thus a deficiency of any of them can lead to oxidative stress on the body.
Vitamin E has been the target of many in vitro and in vivo studies and the subject of controversy for its role in the prevention and cure of a variety of human cardiovascular diseases, including atherosclerosis. Studies have shown that individuals suffering from atherosclerotic diseases have lower vitamin E concentrations than those in the blood of controls.
Vitamin E or in particular the bioactive form, a-tocopherol serves as a selective oxidant trap, reducing the free radical chain-carrying process and producing the ultimate oxidation product, tocopherol tocoquinone. Evidence is accumulating to demonstrate that vitamin E acts in vivo as a selective lipid anti-oxidant in fat-rich cellular membranes. It has the ability to prevent free radical damage to the polyunsaturated fatty acids (PUFA’s) within the phospholipid layer of each cell membrane and the oxidation of Low Density Lipoproteins (LDL).
Because most of the oxidation of LDL occurs in the subendothelial area which is a hydrophobic environment that favours fat soluble antioxidants, it is likely that it will work better here to reduce this oxidation. a-tocopherol acts as a radical sink, by dragging radical reactions from the aqueous phase into the lipoprotein molecule. This effectively means that a tocopherol functions as a pro-oxidant rather than an antioxidant. This in turn aids in reducing the event of atherogenesis from taking place and decreasing the risk and/or progression of cardiovascular disease.
It is important to consider the dosage of vitamin E and at what level it proceeds to reduce the progression of LDL oxidation and atherosclerosis. In a study involving almost 40,000 men aged between 40 and 75, the statistical analysis showed a reduction in coronary disease cases with higher intakes of vitamin E, C and carotene, compared with those consuming lower amounts. The best results were either over 400IU of vitamin E, 19,000IU of beta carotene and 1000mg of vitamin C daily. In this study like others, it is apparent there is less of a reduction in risk for vitamin E and beta carotene for those who choose to smoke.
Studies also suggest that a tocopherol supplementation on its own is not as effective as when it is used in conjunction with co-antioxidants such as ascorbate (vitamin C), beta carotene and co-enzyme Q10. This is understandable when taking into account the effect that ascorbate has on a tocopherol. The mechanism of ascorbate in this instance is in the synergy with vitamin E by regenerating it. With vitamin E being a fat soluble antioxidant and vitamin C being a water soluble antioxidant they are complimentary of each other, which enhances the mopping up of free radicals and reduces LDL oxidation. Vitamin C’s regeneration of vitamin E effectively restores it to its unoxidised state, ready to act as an antioxidant again and again. Not only does vitamin C aid this process, but CO Q10 and glutathione are also involved in recycling vitamin E back to its unoxidised state. It is this collective antioxidant action which protects the cardiovascular system against undue oxidative stress.
There are antioxidants other than vitamin E that play a part in reducing cardiovascular disease due to oxidation. Quercetin is highly antiinflammatory and provides nutritional support for healthy capillary tone. It has been shown to inhibit the oxidation alteration of LDL in vitro. This is possibly due to its ability as a potent antioxidant in its own right and its sparing action on vitamin C. Beta-carotene is a thirst quencher of singlet oxygen and a free radical-trapper antioxidant, as opposed to a-tocopherols chain-breaking effect. CO Q10 is a lipid-soluble antioxidant which prevents damage to DNA, proteins and lipids. Located in the lipid structure of the mitochondrial membranes it is involved in a significant number of reactions, due to the fact that this is a site where large amounts of free radicals are produced. Selenium, similar the other antioxidants also effects cholesterol levels. It is essential for glutathione peroxidase activity and increases the ratio of HDL and LDL while aiding in the prevention of platelet aggregation.
Vitamin C not only has a sparing effect on vitamin E, it strengthens the collagen structures of arteries, lowers total cholesterol and blood pressure while raising high density lipoprotein (HDL) cholesterol levels. One study showed that for every 0.5 milligrams per decilitre increase of vitamin C in the blood, HDL can be increased by 14.9 milligrams per decilitre in women and 2.1 milligrams per decilitre in men. This leads to a decreased risk of heart disease by 4 percent for every 1 percent rise in HDL cholesterol. These results may have been due to a vitamin C deficiency and dose related.
It is important to monitor dose amounts as excess supplementation of one antioxidant may lead to an imbalance in others, especially if there is a deficiency. It appears that the collective antioxidant action protects the cardiovascular system more fully against undue oxidative stress. This is apparent when taking into account the effects that all the antioxidants have on each other and the results of several studies. There are many herbs which also offer good antioxidant protection and having a balanced diet which includes fresh fruit and vegetables will ensure flavonoid antioxidants as well as the other cofactors are available.
Written by Carolyn Fletcher (McSweeney). Carolyn is a Clinical Medical Herbalist, Clinical Nutritionist, Neuro-linguistic Programming (NLP) Master Practitioner, HNLP Coach/Counsellor, Live Blood Analysist and has a National Certificate in Adult Education and Training.