Your body needs to maintain a certain balance between free radicals and antioxidants. When this equilibrium is disrupted, it can lead to oxidative stress.

Plants and animals, as well as all other forms of life, have their own defenses against free radicals and oxidative damage. Adequate antioxidant intake is important. In fact, your life depends on the intake of certain antioxidants — namely, vitamins C and E.

However, many other non-essential antioxidants occur in food. The health benefits associated with a diet rich in plants is at least partially due to the variety of antioxidants they provide Berries, green tea , coffee, and dark chocolate are renowned for being good sources of antioxidants Meat products and fish also contain antioxidants, but to a lesser extent than fruits and vegetables 15 , Antioxidants can increase the shelf life of both natural and processed foods.

For instance, vitamin C is often added to processed foods to act as a preservative Your diet is an essential source of antioxidants, which are found in animal and plant foods — especially vegetables, fruits, and berries. Water-soluble antioxidants perform their actions in the fluid inside and outside cells, whereas fat-soluble ones act primarily in cell membranes.

Notable examples include curcuminoids in turmeric and oleocanthal in extra virgin olive oil. These substances function as antioxidants but also have potent anti-inflammatory activity 19 , Some studies even show that high doses of antioxidants increase your risk of death 23 , For this reason, most health professionals advise people to avoid high-dose antioxidant supplements , although further studies are needed before solid conclusions can be reached.

Eating plenty of antioxidant-rich whole food is a much better idea. Studies indicate that foods reduce oxidative damage to a greater extent than supplements.

For example, one study compared the effects of drinking blood-orange juice and sugar water, both of which contained equal amounts of vitamin C. It found that the juice had significantly greater antioxidant power The best strategy to ensure adequate antioxidant intake is to follow a diet rich in various vegetables and fruits, alongside other healthy habits However, low-dose supplements, such as multivitamins, may be beneficial if you are deficient in certain nutrients or unable to follow a healthy diet.

Studies suggest that taking regular, high-dose antioxidant supplements may be harmful. If possible, get your daily dose of antioxidants from whole foods, such as fruits and vegetables. Adequate antioxidant intake is essential to a healthy diet, although some studies suggest that high-dose supplements may be harmful.

The best strategy is to get your daily dose of antioxidants from healthy plant foods, such as fruits and vegetables. Our experts continually monitor the health and wellness space, and we update our articles when new information becomes available.

Table of contents 20 chapters Search within book Search. Page 1 Navigate to page number of 2. Front Matter Pages i-xxix. Introducing Chapter: Phytochemicals, Antioxidant Therapy, Opportunities and Challenges Kaïs Hussain Al-Gubory Pages Plants of Indian Traditional Medicine with Antioxidant Activity Abhishek Das, Dipankar Chaudhuri, Rhitajit Sarkar, Nikhil Baban Ghate, Sourav Panja, Nripendranath Mandal Pages Antioxidant Potential of African Medicinal Plants Ashwell Rungano Ndhlala, Bhekumthetho Ncube, Hafiz Ahmed Abdelgadir, Christian Phillipus Du Plooy, Johannes Van Staden Pages Plant-Based Diets for Health Maintenance and Disease Prevention: Why and How?

Kaïs Hussain Al-Gubory Pages Antioxidants in Reproductive Health and Fertility Rachel L. Darché, Elizabeth H. Ruder, Jeffrey Blumberg, Terryl J. Hartman, Marlene B. Goldman Pages Antioxidant Therapy in Assisted Reproductive Technologies Ashok Agarwal, Damayanthi Durairajanayagam Pages Plant Antioxidants in the Prevention of Early Life Programming Diseases Kaïs Hussain Al-Gubory Pages Antioxidants Against Environmental Factor-Induced Oxidative Stress Jorge H.

Limón Pacheco, Marta A. Carballo, María E. Gonsebatt Pages Antioxidant Therapy Against Persistent Organic Pollutants and Associated Diseases Bernhard Hennig, Michael C.

Petriello, Bradley J. Newsome, Jordan T. Perkins, Dandan Liu Pages Antioxidants in Physical Exercise and Sports Performance Li Zuo, Tingyang Zhou, Chia-Chen Chuang Pages Plant Polyphenols in Healthcare and Aging Kanti Bhooshan Pandey, Syed Ibrahim Rizvi Pages Free Radicals and Antioxidants in Human Disease Michael Lawson, Klaudia Jomova, Patrik Poprac, Kamil Kuča, Kamil Musílek, Marian Valko Pages Protective Effects of Dietary Polyphenols in Human Diseases and Mechanisms of Action Tao Shen, Xiu-Zhen Han, Xiao-Ning Wang, Pei-Hong Fan, Dong-Mei Ren, Hong-Xiang Lou Pages Plant Flavonoids in Health, Prevention, and Treatment of Chronic Diseases Aleksandra Kozłowska, Dorota Szostak-Węgierek Pages Dietary Polyphenols in the Prevention and Treatment of Diabetes Mellitus Kanwal Rehman, Kaïs Hussain Al-Gubory, Ismail Laher, Muhammad Sajid Hamid Akash Pages Jump to: — What are antioxidants?

Another constant threat comes from chemicals called free radicals. In very high levels, they are capable of damaging cells and genetic material.

The body generates free radicals as the inevitable byproducts of turning food into energy. Free radicals are also formed after exercising or exposure to cigarette smoke, air pollution, and sunlight. Free radicals come in many shapes, sizes, and chemical configurations.

What they all share is a voracious appetite for electrons, stealing them from any nearby substances that will yield them. Free radical damage can change the instructions coded in a strand of DNA. It can make a circulating low-density lipoprotein LDL, sometimes called bad cholesterol molecule more likely to get trapped in an artery wall.

An excessive chronic amount of free radicals in the body causes a condition called oxidative stress, which may damage cells and lead to chronic diseases. The body, long used to this relentless attack, makes many molecules that quench free radicals as surely as water douses fire.

We also extract free-radical fighters from food. They are also involved in mechanisms that repair DNA and maintain the health of cells. There are hundreds, probably thousands, of different substances that can act as antioxidants. The most familiar ones are vitamin C , vitamin E , beta-carotene , and other related carotenoids, along with the minerals selenium and manganese.

Most are naturally occurring, and their presence in food is likely to prevent oxidation or to serve as a natural defense against the local environment. It is really a chemical property, namely, the ability to act as an electron donor. Some substances that act as antioxidants in one situation may be pro-oxidants—electron grabbers—in a different situation.

Another big misconception is that antioxidants are interchangeable. Each one has unique chemical behaviors and biological properties. They almost certainly evolved as parts of elaborate networks, with each different substance or family of substances playing slightly different roles.

This means that no single substance can do the work of the whole crowd. Antioxidants came to public attention in the s, when scientists began to understand that free radical damage was involved in the early stages of artery-clogging atherosclerosis.

It was also linked to cancer , vision loss, and a host of other chronic conditions. Some studies showed that people with low intakes of antioxidant-rich fruits and vegetables were at greater risk for developing these chronic conditions than were people who ate plenty of those foods.

Clinical trials began testing the impact of single substances in supplement form, especially beta-carotene and vitamin E, as weapons against chronic diseases. Supplement makers touted the disease-fighting properties of all sorts of antioxidants.

The research results were mixed, but most did not find the hoped-for benefits. Antioxidants are still added to breakfast cereals, sports bars, energy drinks, and other processed foods , and they are promoted as additives that can prevent heart disease, cancer, cataracts, memory loss, and other conditions.

Randomized placebo-controlled trials, which can provide the strongest evidence, offer little support that taking vitamin C, vitamin E, beta-carotene, or other single antioxidants provides substantial protection against heart disease, cancer, or other chronic conditions.

The results of the largest trials have been mostly negative. A modest effect of vitamin E has been found in some studies but more research is needed.

A study from the Journal of Respiratory Research found that different isoforms of vitamin E called tocopherols had opposing effects on lung function. Lung function was tested using spirometric parameters: higher parameters are indicative of increased lung function, while lower parameters are indicative of decreased lung function.

The study found that higher serum levels of alpha-tocopherol were associated with higher spirometric parameters and that high serum levels of gamma-tocopherol were associated with lower spirometric parameters.

Though the study was observational in nature, it confirmed the mechanistic pathway of alpha- and gamma-tocopherol in mice studies. When it comes to cancer prevention, the picture remains inconclusive for antioxidant supplements. Few trials have gone on long enough to provide an adequate test for cancer.

High-dose antioxidant supplements can also interfere with medicines. Vitamin E supplements can have a blood-thinning effect and increase the risk of bleeding in people who are already taking blood-thinning medicines.

Some studies have suggested that taking antioxidant supplements during cancer treatment might interfere with the effectiveness of the treatment. Inform your doctor if starting supplements of any kind.

One possible reason why many studies on antioxidant supplements do not show a health benefit is because antioxidants tend to work best in combination with other nutrients, plant chemicals, and even other antioxidants. For example, a cup of fresh strawberries contains about 80 mg of vitamin C, a nutrient classified as having high antioxidant activity.

Polyphenols also have many other chemical properties besides their ability to serve as antioxidants. There is a question if a nutrient with antioxidant activity can cause the opposite effect with pro-oxidant activity if too much is taken.

This is why using an antioxidant supplement with a single isolated substance may not be an effective strategy for everyone. Differences in the amount and type of antioxidants in foods versus those in supplements might also influence their effects.

For example, there are eight chemical forms of vitamin E present in foods. However, vitamin E supplements typically only include one form, alpha-tocopherol.

Epidemiological prospective studies show that higher intakes of antioxidant-rich fruits, vegetables, and legumes are associated with a lower risk of chronic oxidative stress-related diseases like cardiovascular diseases , cancer, and deaths from all causes.

The following are nutrients with antioxidant activity and the foods in which they are found:. Excessive free radicals contribute to chronic diseases including cancer, heart disease, cognitive decline, and vision loss.

Keep in mind that most of the trials conducted have had fundamental limitations due to their relatively short duration and inclusion of people with existing disease. At the same time, abundant evidence suggests that eating whole in fruits , vegetables , and whole grains —all rich in networks of naturally occurring antioxidants and their helper molecules—provides protection against many scourges of aging.

The contents of this website are for educational purposes and are not intended to offer personal medical advice. You should seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition.

Never disregard professional medical advice or delay in seeking it because of something you have read on this website.

However, the damage caused by an overload of free radicals over time may become irreversible and lead to certain diseases including heart and liver disease and some cancers such as oral, oesophageal, stomach and bowel cancers.

Oxidation can be accelerated by stress , cigarette smoking , alcohol , sunlight, pollution and other factors. Antioxidants are found in certain foods and may prevent some of the damage caused by free radicals by neutralising them. These include the nutrient antioxidants, vitamins A, C and E, and the minerals copper, zinc and selenium.

Other dietary food compounds, such as the phytochemicals in plants, are believed to have greater antioxidant effects than vitamins or minerals. These are called the non-nutrient antioxidants and include phytochemicals, such as lycopenes in tomatoes and anthocyanins found in cranberries.

A diet high in antioxidants may reduce the risk of many diseases including heart disease and certain cancers. Antioxidants scavenge free radicals from the body cells and prevent or reduce the damage caused by oxidation.

The protective effect of antioxidants continues to be studied around the world. For instance, men who eat plenty of the antioxidant lycopene found in red fruits and vegetables such as tomatoes, apricots, pink grapefruit and watermelon may be less likely than other men to develop prostate cancer.

Lycopene has also been linked to reduced risk of developing type 2 diabetes mellitus. Lutein, found in spinach and corn, has been linked to a lower incidence of eye lens degeneration and associated vision loss in the elderly.

Research also suggests that dietary lutein may improve memory and prevent cognitive decline. Studies show that flavonoid-rich foods prevent some diseases, including metabolic-related diseases and cancer.

Apples, grapes, citrus fruits, berries, tea, onions, olive oil and red wine are the most common sources of flavonoids. Plant foods are rich sources of antioxidants. They are most abundant in fruits and vegetables, as well as other foods including nuts, wholegrains and some meats, poultry and fish.

Good sources of specific antioxidants include:. There is increasing evidence that antioxidants are more effective when obtained from whole foods, rather than isolated from a food and presented in tablet form.

Research shows that some vitamin supplements can increase our cancer risk. For example, vitamin A beta-carotene has been associated with a reduced risk of certain cancers, but an increase in others — such as lung cancer in smokers if vitamin A is purified from foodstuffs. A study examining the effects of vitamin E found that it did not offer the same benefits when taken as a supplement.

A well-balanced diet, which includes consuming antioxidants from whole foods, is best. If you need to take a supplement, seek advice from your doctor or dietitian and choose supplements that contain all nutrients at the recommended levels.

Understanding the protective versus the damaging effects of reactive oxygen species could be the key to developing a safe and effective antioxidant therapy that lowers the risk of certain diseases.

Wojtovich and Thomas Foster, Ph. elegans , an organism that has many similarities to mammals. and Paul Brookes, Ph. Berk, M. Wojtovich will be presenting a seminar on this work at the University of Rochester Genetics Day on Friday, May Some investigators have concluded that, because treatment with one compound with antioxidant properties fails to show benefit in a particular disease, "antioxidant therapy does not benefit this disease," or that oxidative mechanisms are not important in pathophysiology.

Combination therapy with vitamin E and selegiline did not provide an additional benefit compared with either alone. In another small trial in Huntington disease using a different antioxidant, treatment of 48 patients with idebenone at 90 mg three times per day for 1 year failed to provide obvious clinical benefit compared with 43 patients treated with placebo.

Apart from trial size, there are several other reasons why trials with antioxidants in neurodegenerative diseases such as Huntington disease would not appear to demonstrate a positive outcome, even if oxidative damage plays a role in the pathophysiology of the disease.

If the mechanisms underlying the disease are multiple and redundant, and neuronal injury occurs as a consequence of a number of concurrent or sequential processes, antioxidant therapy alone may not be effective.

Protection against one pathway of cell damage may not be enough to halt disease progression. Multiple modes of therapy may be needed for an appreciable clinical effect in complex neurological disorders, eg, the combined use of potent antioxidants, N -methyl D-aspartate NMDA and non-NMDA receptor antagonists, inhibitors of apoptosis, and centrally acting calcium channel blockers.

Furthermore, multimodal therapy may need to be delivered in a specific temporal sequence depending on the time course of various pathogenetic mechanisms of cellular injury, eg, following head injury. In addition, therapy may start too late in the course of an established disease process to demonstrate a clinical effect, as the pathologic effects of many neurodegenerative disorders are well advanced at the time of clinical presentation.

The two children who did not respond were identified as noncompliant with therapy, and this was confirmed by the measurement of plasma vitamin E levels. None of the 12 children given placebo showed any improvement in seizure frequency. To our knowledge, the encouraging results of this trial have not been replicated in a larger study.

Tirilazad mesylate, a aminosteroid that inhibits lipid peroxidation, 55 has been studied in 4 acute neurologic disorders, with mixed results. Interestingly and somewhat surprisingly, two very similar large trials of tirilazad in subarachnoid hemorrhage, one in Europe, Australia, and New Zealand and the other in North America, have provided conflicting results.

In the North American study, 58 no difference was detected between those given the same dose of tirilazad and placebo. Although the reason for the different results of these 2 trials is unclear, it may be related to the fact that significantly more patients in the North American trial were treated with phenytoin, which is known to decrease the bioavailability of tirilazad.

In acute spinal cord injury, treatment with tirilazad mesylate, 2. Perturbations in oxidative metabolism and increased oxidative stress may underlie neuronal degeneration in ALS. Extract of the plant Gingko biloba is a popular complementary remedy marketed for use for a variety of disorders, including supposed enhancing effects on cognition.

Its beneficial effects are believed to derive in part from its high antioxidant flavonoid and terpenoid content. Two trials from Japan have recently been reported using the novel antioxidant ebselen, a compound with an action similar to that of glutathione peroxidase.

Post hoc analysis showed that the improvement occurred especially in those in whom treatment was initiated within 24 hours.

In patients with subarachnoid hemorrhage, treatment with ebselen initiated within 96 hours using a dose schedule similar to that in the ischemic stroke trial improved the outcome at 3 months in those patients 58 in the placebo group, 52 in the ebselen group who suffered neurologic deficit secondary to vasospasm, and this improvement correlated with findings on computed tomography.

Two small studies of antioxidant therapy in patients with human immunodeficiency virus—associated cognitive impairment have been published. The vitamin E analogue OPC was as well tolerated as placebo in a study of 30 patients, and despite the trial limitations, there was a trend toward improved cognitive test scores in the treated group.

A large body of evidence suggests that oxidative injury is important in either the primary or downstream secondary pathophysiological mechanisms underlying many neurologic disorders, and that therapy with appropriate antioxidants may be beneficial. However, the clinical trials performed to date provide conflicting data.

There are several potential reasons for this, including suboptimal dose schedules, the inappropriate use of a particular antioxidant for a given disease, and the redundancy of disease pathophysiology.

Measurement of novel indices of free radical injury now available should be used to provide biochemical evidence of antioxidant effectiveness and to provide surrogate markers of efficacy in clinical trials. To date, trial planners may not have adequately considered the complex biochemistry of free radical biology.

In the future, the availability of potential screening strategies to identify subjects at risk for some disorders may compel us to study the potential utility of predisease antioxidant therapy. Identification of high-risk individuals is now possible for Huntington disease and forms of Alzheimer disease due to autosomal dominant gene mutations.

Advances in molecular neurogenetics may soon allow us to identify many diseases of the nervous system at the preclinical stage. The ethics of such selective screening and the design of testable early treatment strategies in asymptomatic individuals, including antioxidant therapies, is one of the important issues facing neurology in this new millenium.

We thank Arthur Asbury, MD, Christopher Clark, MD, and Garret FitzGerald, MD, for reviewing the manuscript and for their helpful comments. Corresponding author: Norman Delanty, Department of Clinical Neurological Sciences, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin 9, Ireland e-mail: normandelanty eircom.

full text icon Full Text. Download PDF Top of Article Abstract Antioxidants Clinical trials of antioxidants in neurology Clinical trials with vitamin e therapy as the main intervention Clinical trials with tirilazad Other antioxidant trials Conclusions Article Information References.

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