Contact Us



Replenishing the Aging Body’s Antioxidant Defenses

By Laurie Barclay, MD

One of the most important ways to protect against premature aging is maintaining the integrity of the cell’s lipid membrane and DNA. Maintaining these vital cellular structures enhances the body’s ability to guard against age-related disease, including the well-known destructive effects inflicted by free radicals.1,2


A critical defense against free-radical damage is the body’s own internally generated antioxidant enzyme known as superoxide dismutase (SOD). This powerful enzyme, which functions both within and outside of cell membranes, greatly reduces oxidative stress and inflammation that can lead to atherosclerosis, arthritis, cognitive impairment, and other age-related afflictions.3-5 Unfortunately, levels of SOD dramatically decrease with advancing age, thereby limiting our natural ability to ward off degenerative disease.

Intriguing new research suggests that a Chinese herb known as wolfberry

can enhance the activity of superoxide dismutase throughout the body.6,7 Combined with other proven SOD-boosting nutrients, wolfberry, an edible fruit, can help restore youthful SOD levels and optimal antioxidant defenses.

In this article, we reveal how to supercharge the production of powerful internal antioxidants (like SOD) to help you guard against oxidative stress and inflammation, while enhancing strength, vigor, and longevity.

SOD Disarms Dangerous Superoxide Radicals

While essential to life, oxygen also generates toxic byproducts known as reactive oxygen species, or free radicals. Both normal aging and chronic disease dramatically increase the production of free radicals,8,9 which can severely damage DNA, proteins, and lipids needed for cell growth, reproduction, metabolism, and repair.1 The result of all this cellular damage can range from atherosclerosis to cancer and even Alzheimer’s.10,11

Each day, our bodies fight off these damaging free radicals with the help of superoxide dismutase (SOD), which helps break down free radicals so that they are eventually converted into harmless water and oxygen.12

Improved Bioavailability Enhances SOD’s Effectiveness

Until recently, supplementing with SOD from food sources has been almost impossible. Digestive enzymes in the stomach quickly break down and deactivate orally ingested SOD. To create a more bioavailable form of SOD, researchers have coupled the SOD protein molecule to a carrier protein known as gliadin, derived from plant sources. Like a protective convoy, gliadin ushers SOD past the destructive stomach enzymes and delivers it to the intestines, where it is then absorbed directly into the bloodstream.13

Scientists began experiments with this new form of SOD coupled with gliadin (GliSODin®) to measure its absorption and utilization in the body. In one study, GliSODin® was associated with significantly increased activity of circulating antioxidant enzymes. Additionally, researchers noted that GliSODin® enhanced anti-inflammatory activity and improved the resistance of red blood cells to rupture induced by oxidative stress. This led scientists to conclude that supplementation with GliSODin® improves cellular antioxidant status while protecting against cell death induced by oxidative stress.13,14

The SOD-gliadin combination was shown to exert beneficial effects in cancer prevention as well. In an experimental model of tumor development, about 80% of laboratory animals given oral gliadin alone developed cancer, compared to only 40% of those given an oral SOD-gliadin compound. Moreover, cancer cells from subjects given SOD-gliadin were much less likely to spread (metastasize) than were cancer cells from those given gliadin alone. The researchers attributed the SOD-gliadin combination’s remarkable anti-cancer effects to SOD’s ability to scavenge the inflammatory superoxide radical.15

Clinical Studies Confirm Benefits of SOD-Boosting Supplements

In clinical as well as laboratory studies, supplements that boost SOD activity in the body show tremendous therapeutic potential.

Two studies sponsored by Life Extension examined SOD’s benefits in humans using SODzyme™, an extract derived from the sprouts of corn, soy, and wheat.16,17 In an open-label study, 12 middle-aged volunteers given 2000 mg of SODzyme™ daily for two weeks had a 30% increase in serum SOD levels and a 47% decrease in blood levels of hydrogen peroxide, a compound that aggravates inflammation associated with arthritis. These volunteers not only experienced a restoration of SOD to levels typically seen in much younger adults, but also had a 47% increase in the activity of a vital antioxidant enzyme known as catalase.16

In the second pilot study, 30 adults with arthritis or other inflammatory conditions received placebo or SODzyme™ for four weeks. A validated test designed to evaluate pain showed an impressive 71% decrease in pain in the SODzyme™ group and no change in the placebo group. Interestingly, patients who had the most pain when the study began achieved the greatest pain relief with SODzyme™. Several patients with various forms of painful arthritis or joint injury reported dramatic improvements in (and even absence of) pain within one to two weeks of starting SODzyme™, with no return in pain at the three-month follow-up and an improved ability to return to usual activities.17

SODzyme™ also demonstrates an impressive safety record. Unlike conventional nonsteroidal anti-inflammatory drugs (NSAIDs) or COX-2 inhibitors such as Celebrex® that are used to treat arthritis and inflammatory pain, SOD-boosting supplements have no adverse gastrointestinal or cardiovascular effects, due to their different mechanism of action.18

SOD’s versatility is demonstrated by its ability to protect the skin against damage caused by ultraviolet light. In a randomized, double-blind, placebo-controlled study, scientists exposed the forearms of 50 volunteers to ultraviolet light once a week for four weeks. Starting two to three days before the first exposure, the participants took a daily supplement containing either GliSODin® or placebo. Individuals receiving GliSODin®, even those with fair skin, were able to withstand eight times more ultraviolet light exposure before they developed sunburn compared to those who received placebo. Other benefits of GliSODin® were less skin inflammation and more rapid healing of redness after burning occurred. The scientists concluded that GliSODin® effectively prevents the consequences of oxidative stress resulting from excessive sun exposure, and that this effect is particularly important for fair-skinned individuals.19

For many patients suffering from burns or diabetic wounds, hyperbaric (high-pressure) oxygen can significantly contribute to faster healing. However, such treatment with high-pressure oxygen can result in breaks in DNA strands while increasing levels of isoprostanes, which reflect oxidative damage to cellular membranes. Studies show that oral antioxidants such as vitamin E and N-acetylcysteine do not protect against the unique type of oxidative damage associated with hyperbaric oxygen treatment.20 The combination of SOD and gliadin, however, offers effective protection against the oxidative stress of hyperbaric oxygen.

In a randomized, double-blind, placebo-controlled study, 20 volunteers each received an hour of hyperbaric oxygen treatment. Those who supplemented with SOD-gliadin had significantly decreased oxidative damage and fewer DNA breaks, as well as less elevation of isoprostane levels. SOD thus appears to have great therapeutic value for people exposed to extreme oxidative stress.21 Since other antioxidants did not protect against the damage induced by hyperbaric oxygen, researchers have proposed that SOD’s beneficial effects are specific and not related solely to its antioxidant activity.20

These studies offer powerful evidence that supplements that boost SOD levels and activity in the body confer significant protection against damage to DNA, lipids, and skin, while relieving pain and inflammation.

SOD and Wolfberry: What You Need to Know
  • The antioxidant superoxide dismutase (SOD) works at the molecular level to disarm the superoxide radical and protect against cellular damage.
  • Although SOD was previously unavailable as dietary supplement, scientists have recently developed an orally bioavailable SOD formulation that boosts blood levels of SOD.
  • Potential benefits of orally available SOD include relieving inflammation and pain, enhancing cellular life span, and protecting against conditions ranging from diabetes and cancer to cardiovascular and neurodegenerative disorders.
  • The Chinese herbal remedy wolfberry is rich in potent antioxidants and enhances SOD activity in the body.
  • Wolfberry’s therapeutic applications include relieving fatigue, promoting visual health, protecting against diabetes, enhancing male sexual function, and supporting a healthy life span.
  • Combining orally available SOD with wolfberry is an effective way to boost the body’s SOD levels and activity, with benefits for disease protection, youthful energy, and longevity.

Wolfberry Boosts SOD Activity to Fight Biological Aging

Laboratory analysis has shown that an exotic fruit known as wolfberry is one of nature’s most concentrated sources of antioxidants. Moreover, emerging research suggests that wolfberry’s antioxidant properties may be attributable to its ability to increase the availability of SOD throughout the body.

For nearly 2,000 years, wolfberry has been used in traditional Chinese medicine to improve immune system function, vision, circulation, and sperm production, as well as to detoxify and protect the liver. Traditional Chinese medicine holds that wolfberry may also improve life span, sexual energy, vigor, and muscular strength, while reducing pain and protecting against cancer, inflammation, and viral infection.6

The abundance of nutrients and antioxidants packed into the tiny wolfberry include plant-derived polyphenolic antioxidants; carotenoids such as beta-carotene, zeaxanthin, lutein, beta-cryptoxanthin, and lycopene; vitamins C, B1, B2, and niacin; more than 30 essential and trace minerals, including zinc, iron, copper, calcium, selenium, and phosphorus; polysaccharides; and 18 amino acids such as isoleucine, tryptophan, leucine, and arginine.

Wolfberry’s antioxidant activity is likely attributable in part to its carotenoids, phenolics, and vitamin C.44 Compared to other highly potent antioxidants derived from traditional Chinese herbs, wolfberry is even more effective in scavenging superoxide radicals and preventing their formation. Based on these observations, scientists believe that wolfberry dietary supplements represent an important source of daily antioxidant intake.45

Wolfberry’s powerful antioxidant effects, however, may also arise from its ability to boost SOD’s activity in the body. Wolfberry accelerates the rate of biochemical reactions that enable SOD to carry out its essential function of quenching oxidative stress. Since SOD disarms the dangerous superoxide radical to fight inflammation and degenerative diseases, wolfberry may have similar therapeutic effects, protecting against diabetes, sexual dysfunction, and the effects of aging.

One research team tested wolfberry’s effects in oxygen-deprived subjects. Those who received wolfberry demonstrated higher SOD activity and antioxidant capacity than did those deprived of oxygen in the absence of wolfberry.7 Wolfberry thus appears to protect against the damaging effects of ischemia (insufficient oxygen supply).

SOD Protects Against a Host of Degenerative Diseases

While SOD has been linked to youthfulness, longevity, and protection against chronic illnesses, the body’s production of SOD drops dramatically with advancing age.2 Conditions associated with free-radical damage that may benefit from increased SOD levels include a host of inflammatory and degenerative diseases:

  • Nowhere are the signs of aging more visible than in the skin, where the effects of free-radical damage accumulate and produce visible signs of skin aging. SOD may help to protect against age-related skin wrinkling by arresting the breakdown of collagen, an essential protein that tones and strengthens the skin.22
  • A chronic illness with many serious complications, diabetes is associated with increased oxidative stress. Increasing SOD levels may help fight the onset and progression of diabetes.23
  • SOD’s powerful antioxidant properties could have important therapeutic applications in preventing and managing cancer.24-26 Scientists now believe that genetically based deficiencies of SOD are linked to an increased susceptibility of certain people to breast and pancreatic cancers.24,25 Ensuring adequate SOD levels may help protect against these potentially deadly malignancies.
  • By shielding the body from superoxide radicals, SOD may help prevent the cellular and tissue damage associated with cardiovascular disease.27-29 While mainstream medicine promotes high cholesterol as the primary culprit in atherosclerosis and cardiovascular disease, low levels of SOD and other antioxidants may be even more important factors in elevating cardiovascular risk.30 Providing the body with optimal antioxidant support could protect against America’s leading cause of premature death.
  • The nervous system is highly susceptible to oxidative stress. Because of its ability to protect against superoxide radicals, SOD may guard against the cellular and tissue damage tied to neurological disease.27 Specific neurological diseases linked to abnormalities in SOD include multiple sclerosis31 and Alzheimer’s and Parkinson’s diseases.32-34
  • Superoxide radicals help perpetuate the chronic pain associated with inflammation. SOD’s ability to neutralize superoxide radicals is associated with pain relief,35 with potential benefits for numerous conditions, including fibromyalgia, a chronic source of muscle pain.36
  • Superoxide radicals also underlie the pain and inflammation of arthritis. Research demonstrates that patients with rheumatoid arthritis have lower dietary levels and reduced activity of SOD and glutathione peroxidase (a related antioxidant enzyme) than do healthy subjects.37 Rheumatoid arthritis sufferers also exhibit lower levels of SOD in joint-cushioning cartilage cells known as chondrocytes, leaving these cells vulnerable to the damaging effects of nitric oxide and oxygen radicals.38,39 These findings suggest that depleted levels of critical antioxidants such as SOD perpetuate crippling rheumatoid arthritis.
  • Scientists have linked inflammation to many chronic diseases that accompany aging. Both in cells grown in the laboratory and in live animals, SOD improved the function of white blood cells of the immune system known as macrophages. Although macrophages subjected to oxidative stress release the inflammatory compound called tumor necrosis factor, those treated with SOD release the anti-inflammatory cytokine interleukin-10 (IL-10) instead.14
  • Studies have shown that people who reach the age of 90 or 100 have high blood levels of IL-10, which may protect them from the ravages of aging and from developing cancer by reducing inflammation.40 By promoting the release of IL-10, SOD may help the body ward off inflammation, in a manner similar to that seen in individuals who survive to a very old age.
  • Other studies similarly suggest that SOD may be an important determinant of life span and longevity. Among various mammal species, those that produce higher tissue and serum levels of SOD live longer than those who do not.41,42 This findings suggests that boosting SOD levels may be an important strategy for extending the healthy human life span.

In sum, a wealth of scientific evidence indicates that optimizing SOD levels may help to avert the many diseases associated with inflammation and aging,43 including diabetes, heart disease, neurological conditions, cancer, skin aging, and arthritis.

Wolfberry’s capacity to boost SOD activity may benefit the pancreas, the insulin-producing organ that malfunctions in diabetes. When pancreatic cells were exposed to alloxan (a drug that instigates diabetes by generating superoxide radicals), their protective SOD activity declined dramatically. Adding wolfberry polysaccharides to the oxidative stress-damaged pancreatic cells helped to preserve the cells’ essential SOD activity, thus conferring protection against damaging agents that may contribute to the development of diabetes.46

Wolfberry’s effects in neutralizing oxidative stress may offer additional benefits for diabetes management. Scientists induced diabetes and high cholesterol in test animals by exposing them to alloxan. After the subjects were treated with wolfberry juice or polysaccharides for 10 days, they demonstrated several beneficial changes in blood chemistry markers, including reductions in blood sugar, serum total cholesterol, and triglycerides, and marked increases in beneficial high-density lipoprotein (HDL).47 In this study, wolfberry polysaccharides and amino acids had the greatest effect on blood sugar, whereas wolfberry polysaccharides and antioxidants showed the most benefit on blood lipids.47 Previous studies have shown that wolfberry polysaccharides produce beneficial reductions in potentially dangerous low-density lipoprotein (LDL),48 and that wolfberry flavonoids help limit lipid peroxidation caused by oxygen radicals.49 These studies suggest that wolfberry provides a host of protective benefits against biochemical agents that instigate diabetes and contribute to its damaging effects in the body.

To assess whether wolfberry enhances male sexual performance and fertility, Chinese scientists administered wolfberry extract to partially castrated male rats and mouse testicular cells in the laboratory. Compared to control animals, the partially castrated male rats treated with wolfberry demonstrated higher SOD activity, enhanced secretion of sex hormones, increased testicular weight, and improved sperm quantity and quality. Wolfberry boosted their sexual performance and reproductive function, and also protected the DNA of mouse testicular cells against oxidative damage caused by hydrogen peroxide, with higher doses proportionately more effective than lower doses.50 These findings support wolfberry’s reputation as an aphrodisiac and fertility-facilitating agent, providing a modern scientific rationale for wolfberry’s centuries-old use in managing infertility and promoting sexual health in males.

Wolfberry’s ability to boost SOD activity may even help prevent visible signs of aging. In a research model of skin aging, an extract of wolfberry and bergamot (sour orange) significantly increased both SOD activity and collagen content in the skin. This same botanical combination also promoted hair growth.51 Other studies of aging subjects have shown that treatment with wolfberry increased SOD activity in red blood cells while decreasing levels of harmful compounds in the skin.52 In human skin cells, wolfberry extract has displayed important skin-protective properties.53 These studies indicate that extracts of wolfberry contribute to healthy skin and hair.

Modern Science Confirms Wolfberry’s Health Benefits

Scientific studies have confirmed that wolfberry offers a wealth of health-enhancing benefits: promoting youthful energy, preserving vision, optimizing brain health, increasing longevity, and protecting against conditions related to oxidative stress.

  • All too many people suffer from waning energy levels as they grow older. New evidence suggests that wolfberry extract may help aging adults restore youthful energy levels. When test subjects consumed wolfberry, they became highly resistant to fatigue and were able to endure a greater exercise load. When the subjects did become fatigued, they recovered much more quickly. Scientists determined that this greater resilience was related to an increased ability to store glycogen (a form of glucose energy) in the muscles and liver. Glycogen helps provide the energy required for exercise and strenuous activity, and supports the elimination of metabolic wastes following exercise. Wolfberry thus helps the body to fuel itself for high-energy activity.54
  • As a rich source of the nutrients known to support eye health, wolfberry may offer powerful protection for healthy vision. People seeking to maintain healthy visual function with aging often supplement with zinc and other minerals, carotenoids, and vitamin C, all of which are found in naturally high concentrations in wolfberry. Compared to other plant foods thought to help prevent age-related vision loss, wolfberry has the highest concentration of the dietary carotenoid zeaxanthin.55 Along with lutein, zeaxanthin accumulates in the macula, the region of the eye’s retina responsible for detailed vision. Zeaxanthin is believed to protect against oxidative damage caused by exposure to ultraviolet light. This photoexposure is a major culprit in age-related macular degeneration, one of the most common causes of irreversible vision loss with aging. When 14 volunteers consumed 15 grams of wolfberry daily for 28 days, they demonstrated dramatically increased blood levels of zeaxanthin, about 2.5-fold higher.56 Scientists believe that increased intake of foods containing zeaxanthin may be effective in preventing age-related macular degeneration. Wolfberry may be an ideal choice, since a modest daily intake provides bioavailable zeaxanthin that markedly increases plasma zeaxanthin levels.
  • In addition to its benefits for the body, wolfberry may help keep the mind young. In a research model of cognitive aging, treatment with wolfberry was associated with enhanced learning ability and improved memory capacity.52 Wolfberry may also protect against Alzheimer’s disease, the most common cause of memory-robbing dementia. Using a laboratory model of Alzheimer’s, scientists found that wolfberry protected brain cells from the harmful effects of amyloid beta peptides, damaging agents that are linked to the pathological changes seen in the brains of Alzheimer’s patients. These findings suggest that wolfberry may hold value in preventive or therapeutic strategies for Alzheimer’s disease.57
  • Preliminary laboratory studies suggest other health-promoting applications of wolfberry. Utilizing a model of aging, researchers found that wolfberry increased the rate at which cells produced the genetic material DNA, while prolonging the cells’ life span. Agents that extend the lives of cells could one day find applications in lengthening human life spans.58
  • Evidence from the laboratory and early clinical studies suggests a potential therapeutic role for wolfberry in preventing and managing diseases associated with oxidative stress. Since oxidative stress plays a role in a vast array of illnesses, this suggests possible applications for wolfberry in averting heart disease, arthritis and other inflammatory diseases, some types of cancer, and premature aging, among other disorders.6,44

Conclusion

Scientists and aging adults increasingly recognize that optimizing the body’s antioxidant defenses is critical to fighting disease and avoiding the effects of biological aging. Superoxide dismutase (SOD) is one of the most powerful antioxidants for fighting inflammation, disease, pain, and the effects of aging. By quenching the dangerous superoxide radical, SOD works at the cellular level to prevent damage to crucial proteins, DNA, and lipids that support essential cellular activities.

Breakthroughs in nutritional science have led to the development of orally ingested, highly bioavailable forms of SOD. Combining orally available SOD with wolfberry offers a highly effective strategy to boost SOD levels and activity in the body. This novel combination protects against pain and inflammation, helps prevent a host of degenerative diseases, restores youthful energy and vitality, and promotes a long and healthy life span.

 

SODzyme® with GliSODin® & Wolfberry
90 vegetarian capsules
Item Catalog Number:
00961

Internally produced antioxidants — including the enzymes superoxide dismutase (SOD) and catalase — are the body’s primary defense against free-radical assault, offering up to thousands of times more protection against certain dangerous free radicals than dietary antioxidants.

The body’s supply of youthful antioxidant enzymes rapidly decreases with age.49, 50 Fortunately, SODzyme® with GliSODin® & Wolfberry combines three advanced ingredients to help replenish the body’s supply of SOD, vastly enhancing its natural antioxidant defenses.

The first nutrient is SODzyme®, a proprietary plant-based extract. In a study of 12 middle-aged volunteers who took 2,000 mg of SODzyme® daily for two weeks, SODzyme® boosted serum SOD levels by 30% on average, and reduced toxic hydrogen peroxide by 47%.51

The second ingredient contained in this formula is GliSODin®, a patented, plant-derived form of SOD. In an animal study, small amounts of orally administered GliSODin® raised blood levels of SOD by 89% and increased catalase levels by 171%!52

The third ingredient provided is a standardized wolfberry (Lycium barbarum) fruit extract. Wolfberry is found to have the highest ORAC values of all fruits, and is effective in scavenging superoxide radicals and in preventing their formation. When given to patients aged 64–80, wolfberry increased blood levels of SOD by 48% and lowered dangerous blood lipid peroxides by 65% in only 10 days!53


Supplement Facts

Serving Size 3 vegetarian capsules

Servings Per Container 30

Amount Per Serving

SODzyme® Proprietary Phytoenzyme Blend (Glycine max, Zea mays, wheat sprout concentrate)

2000 mg

Superoxide Dismutase/Gliadin Complex (GliSODin®) [SOD (Superoxide Dismutase) NBT Enzyme Activity = 100 IU]

100 mg

Wolfberry (Lycium barbarum) extract (fruit) [std. to 20% polysaccharides (20 mg)]

100 mg

Other ingredients: vegetarian capsule, dicalcium phosphate, magnesium stearate, silica.

Contains soybeans and wheat. Contains gluten and corn.
This product contains NO milk, egg, fish, peanuts, crustacean shellfish (lobster, crab, shrimp), tree nuts, yeast, or rice. Contains NO sugar, artificial sweeteners, flavors, colors, or preservatives.

NBT† corresponds to the melon extract quantity inhibiting 50% of NitroBlue Tetrazolium reduction.
Isocell SA, France is the owner of US Patents Nos. 6,045,809 and 6,426,068B1 and trademark of GliSODin®.


Dosage and Use
 

Take three capsules early in the day, preferably on an empty stomach, or as recommended by a healthcare practitioner.


Caution

Do not take if you are allergic to soy, corn, wheat, yeast or gluten.


Warnings
 

Top References

1. Yu BP, Chung HY. Adaptive mechanisms to oxidative stress during aging. Mech Ageing Dev. 2006 May;127(5):436-43.

2. Lishnevskaia VI. The role of free radicals oxidation in the deterioration of haemovascular homeostasis in aging. Adv Gerontol. 2004;13:52-7.

3. Congy F, Bonnefont-Rousselot D, Dever S, Delattre J, Emerit J. Study of oxidative stress in the elderly. Presse Med. 1995 Jul 1-8;24(24):1115-8.

4. Levin ED. Extracellular superoxide dismutase (EC-SOD) quenches free radicals and attenuates age-related cognitive decline: opportunities for novel drug development in aging. Curr Alzheimer Res. 2005 Apr;2(2):191-6.

5. Sampayo JN, Gill MS, Lithgow GJ. Oxidative stress and aging—the use of superoxide dismutase/catalase mimetics to extend lifespan. Biochem Soc Trans. 2003 Dec;31(Pt 6):1305-7.

6. Gross PM, Zhang X, Zhang R. Wolfberry: Nature’s Bounty of Nutrition and Health. Booksurge Publishing; 2006.

7. Li G, Yang J, Ren B, Wang Z. Effect of lycium barbarum L on defending free radicals of mice caused by hypoxia. Wei Sheng Yan Jiu. 2002 Feb;31(1):30-1.

8. Barouki R. Ageing free radicals and cellular stress. Med Sci (Paris). 2006 Mar;22(3):266-72.

9. de Magalhaes JP, Church GM. Cells discover fire: employing reactive oxygen species in development and consequences for aging. Exp Gerontol. 2006 Jan;41(1):1-10.

10. Maier CM, Chan PH. Role of superoxide dismutases in oxidative damage and neurodegenerative disorders. Neuroscientist. 2002 Aug;8(4):323-4.

11. Shin SG, Kim JY, Chung HY, Jeong JC. Zingerone as an antioxidant against peroxynitrite. J Agric Food Chem. 2005 Sep 21;53(19):7617-22.

12. Available at: http://pubs.acs.org/cgi-bin/abstract.cgi/achre4/1972/5/i10/f-pdf/f_ar50058a001.pdf?sessid=6006l3. Accessed October 26, 2006.

13. Vouldoukis I, Conti M, Krauss P, et al. Supplementation with gliadin-combined plant superoxide dismutase extract promotes antioxidant defences and protects against oxidative stress. Phytother Res. 2004 Dec;18(12):957-62.

14. Vouldoukis I, Lacan D, Kamate C, et al. Antioxidant and anti-inflammatory properties of a Cucumis melo LC. extract rich in superoxide dismutase activity. J Ethnopharmacol. 2004 Sep;94(1):67-75.

15. Okada F, Shionoya H, Kobayashi M, et al. Prevention of inflammation-mediated acquisition of metastatic properties of benign mouse fibrosarcoma cells by administration of an orally available superoxide dismutase. Br J Cancer. 2006 Mar 27;94(6):854-62.

16. Life Extension-sponsored study #1. Changes in serum levels of superoxide dismutase and catalase in humans after dietary SODzyme™ supplementation.

17. Life Extension-sponsored study #2. Effects of oral SODzyme™ administration on pain scores in human subjects with arthritis.

18. Chan FK. Primer: managing NSAID-induced ulcer complications—balancing gastrointestinal and cardiovascular risks. Nat Clin Pract Gastroenterol Hepatol. 2006 Oct;3(10):563-73.

19. Available at: www.npicenter.com/anm/templates/newsATemp.aspx?articleid=12601&zoneid=24. Accessed October 13, 2006.

20. Dennog C, Radermacher P, Barnett YA, Speit G. Antioxidant status in humans after exposure to hyperbaric oxygen. Mutat Res. 1999 Jul 16;428(1-2):83-89.

21. Muth CM, Glenz Y, Klaus M, et al. Influence of an orally effective SOD on hyperbaric oxygen-related cell damage. Free Radic Res. 2004 Sep;38(9):927-32.

22. Petersen SV, Oury TD, Ostergaard L, et al. Extracellular superoxide dismutase (EC-SOD) binds to type i collagen and protects against oxidative fragmentation. J Biol Chem. 2004 Apr 2;279(14):13705-10.

23. Abou-Seif MA, Youssef AA. Evaluation of some biochemical changes in diabetic patients. Clin Chim Acta. 2004 Aug 16;346(2):161-70.

24. Cai Q, Shu XO, Wen W, et al. Genetic polymorphism in the manganese superoxide dismutase gene, antioxidant intake, and breast cancer risk: results from the Shanghai Breast Cancer Study. Breast Cancer Res. 2004;6(6):R647-55.

25. Ough M, Lewis A, Zhang Y, et al. Inhibition of cell growth by overexpression of manganese superoxide dismutase (MnSOD) in human pancreatic carcinoma. Free Radic Res. 2004 Nov;38(11):1223-33.

26. Manju V, Balasubramanian V, Nalini N. Oxidative stress and tumor markers in cervical cancer patients. J Biochem Mol Biol Biophys. 2002 Dec;6(6):387-90.

27. Fattman CL, Schaefer LM, Oury TD. Extracellular superoxide dismutase in biology and medicine. Free Radic Biol Med. 2003 Aug 1;35(3):236-56.

28. Morrow JD. Quantification of isoprostanes as indices of oxidant stress and the risk of atherosclerosis in humans. Arterioscler Thromb Vasc Biol. 2005 Feb;25(2):279-86.

29. Fukai T, Folz RJ, Landmesser U, Harrison DG. Extracellular superoxide dismutase and cardiovascular disease. Cardiovasc Res. 2002 Aug 1;55(2):239-49.

30. Zawadzka-Bartczak E. Activities of red blood cell anti-oxidative enzymes (SOD, GPx) and total anti-oxidative capacity of serum (TAS) in men with coronary atherosclerosis and in healthy pilots. Med Sci Monit. 2005 Sep;11(9):CR440-4.

31. Lund-Olesen K. Etiology of multiple sclerosis: role of superoxide dismutase. Med Hypotheses. 2000 Feb;54(2):321-2.

32. Summers WK. Alzheimer’s disease, oxidative injury, and cytokines. J Alzheimers Dis. 2004 Dec;6(6):651-7.

33. Choi J, Rees HD, Weintraub ST, et al. Oxidative modifications and aggregation of Cu,Zn-superoxide dismutase associated with Alzheimer and Parkinson diseases. J Biol Chem. 2005 Mar 25;280(12):11648-55.

34. Hattori N. Etiology and pathogenesis of Parkinson’s disease: from mitochondrial dysfunctions to familial Parkinson’s disease. Rinsho Shinkeigaku. 2004 Apr;44(4-5):241-62.

35. Chung JM. The role of reactive oxygen species (ROS) in persistent pain. Mol Interv. 2004 Oct;4(5):248-50.

36. Bagis S, Tamer L, Sahin G, et al. Free radicals and antioxidants in primary fibromyalgia: an oxidative stress disorder? Rheumatol Int. 2005 Apr;25(3):188-90.

37. Bae SC, Kim SJ, Sung MK. Inadequate antioxidant nutrient intake and altered plasma antioxidant status of rheumatoid arthritis patients. J Am Coll Nutr. 2003 Aug;22(4):311-5.

38. Karatas F, Ozates I, Canatan H, et al. Antioxidant status & lipid peroxidation in patients with rheumatoid arthritis. Indian J Med Res. 2003 Oct;118:178-81.

39. Mazzetti I, Grigolo B, Pulsatelli L, et al. Differential roles of nitric oxide and oxygen radicals in chondrocytes affected by osteoarthritis and rheumatoid arthritis. Clin Sci (Lond). 2001 Dec;101(6):593-9.

40. Caruso C, Lio D, Cavallone L, Franceschi C. Aging, longevity, inflammation, and cancer. Ann NY Acad Sci. 2004 Dec;1028:1-13.

41. Cutler RG. Antioxidants and longevity of mammalian species. Basic Life Sci. 1985;35:15-73.

42. Cutler RG. Antioxidants and aging. Am J Clin Nutr. 1991 Jan;53(1 Suppl):373S-9S.

43. Gow A, Ischiropoulos H. Super-SOD: superoxide dismutase chimera fights off inflammation. Am J Physiol Lung Cell Mol Physiol. 2003 Jun;284(6):L915-6.

44. Young G, Lawrence R, Schreuder M. Discovery of the Ultimate Superfood. Essential Science Publishing; 2005.

45. Wu SJ, Ng LT, Lin CC. Antioxidant activities of some common ingredients of traditional chinese medicine, Angelica sinensis, Lycium barbarum and Poria cocos. Phytother Res. 2004 Dec;18(12):1008-12.

46. Xu M, Zhang H, Wang Y. The protective effects of Lycium barbarum polysaccharide on alloxan- induced isolated islet cells damage in rats. Zhong Yao Cai. 2002 Sep;25(9):649-51.

47. Luo Q, Cai Y, Yan J, Sun M, Corke H. Hypoglycemic and hypolipidemic effects and antioxidant activity of fruit extracts from Lycium barbarum. Life Sci. 2004 Nov 26;76(2):137-49.

48. Huang LJ, Tian GY, Wang ZF, Dong JB, Wu MP. Studies on the glycoconjugates and glycans from Lycium barbarum L in inhibiting low density lipoprotein (LDL) peroxidation. Yao Xue Xue Bao. 2001 Feb;36(2):108-11.

49. Huang Y, Lu J, Shen Y, Lu J. The protective effects of total flavonoids from Lycium Barbarum L. on lipid peroxidation of liver mitochondria and red blood cell in rats. Wei Sheng Yan Jiu. 1999 Mar 30;28(2):115-6.

50. Luo Q, Li Z, Huang X, et al. Lycium barbarum polysaccharides: Protective effects against heat-induced damage of rat testes and H2O2-induced DNA damage in mouse testicular cells and beneficial effect on sexual behavior and reproductive function of hemicastrated rats. Life Sci. 2006 Jul 10;79(7):613-21.

51. Shao LX. Effects of the extract from bergamot and boxthorn on the delay of skin aging and hair growth in mice. Zhongguo Zhong Yao Za Zhi. 2003 Aug;28(8):766-9.

52. Deng HB, Cui DP, Jiang JM, et al. Inhibiting effects of Achyranthes bidentata polysaccharide and Lycium barbarum polysaccharide on nonenzyme glycation in D-galactose induced mouse aging model. Biomed Environ Sci. 2003 Sep;16(3):267-75.

53. Zhao H, Alexeev A, Chang E, Greenburg G, Bojanowski K. Lycium barbarum glycoconjugates: effect on human skin and cultured dermal fibroblasts. Phytomedicine. 2005 Jan;12(1-2):131-7.

54. Luo Q, Yan J, Zhang S. Isolation and purification of Lycium barbarum polysaccharides and its antifatigue effect. Wei Sheng Yan Jiu. 2000 Mar 30;29(2):115-7.

55. Chitchumroonchokchai C, Failla ML. Hydrolysis of zeaxanthin esters by carboxyl ester lipase during digestion facilitates micellarization and uptake of the xanthophyll by Caco-2 human intestinal cells. J Nutr. 2006 Mar;136(3):588-94.

56. Cheng CY, Chung WY, Szeto YT, Benzie IF. Fasting plasma zeaxanthin response to Fructus barbarum L. (wolfberry; Kei Tze) in a food-based human supplementation trial. Br J Nutr. 2005 Jan;93(1):123-30.

57. Yu MS, Leung SK, Lai SW, et al. Neuroprotective effects of anti-aging oriental medicine Lycium barbarum against beta-amyloid peptide neurotoxicity. Exp Gerontol. 2005 Aug;40(8-9):716-27.

58. Wu BY, Zou JH, Meng SC. Effect of wolfberry fruit and epimedium on DNA synthesis of the aging-youth 2BS fusion cells. Zhongguo Zhong Xi Yi Jie He Za Zhi. 2003 Dec;23(12):926-8.



 

Bottom References

Herbal/Phyto Products

1. Am J Clin Nutr. 1985 Jan;41(1):32-6.
2. Ann Epidemiol. 1995 Jul;5(4):255-60.
3. JAMA. 1995 Apr 12;273(14):1113-7.
4. JAMA. 1994 Nov 9;272(18):1413-20.
5. J Natl Cancer Inst. 1995 Dec 6;87(23):1767-76.
6. J Am Diet Assoc. 1996 Oct;96(10):1027-39. Review.
7. http://www.webmd.com/diet/phytonutrients-faq?page=2
8. J Agric Food Chem. 2008 Feb 13;56(3):630-5.
9. Mol Nutr Food Res. 2007 Jun;51(6):652-64.
10. J Agric Food Chem. 2006 Dec 13;54(25):9329-39.
11. Neurobiol Aging. 2005 Dec;26(Suppl 1):128-32.
12. J Agric Food Chem. 2006 Feb 8;54(3):607-16.
13. J Nutr. 2008 Sep;138(9):1692-8.
14. J Food Sci. 2008 Jun;73(5):S215-21.
15. J Food Sci. 2007 Mar;72(2):S167-77.
16. J Agric Food Chem. 2004 Jun 16;52(12):4026-37.
17. Am J Gastroenterol. 1998 Feb;93(2):139-43.
18. Dig Liver Dis. 2004 Nov;36(11):752-9.
19. Life Sci. 1996;58(18):1591-600.
20. Clin Cancer Res. 2005 Dec 1;11(23):8441-8.
21. Altern Med Rev. 2005 Sep;10(3):193-203.
22. Carcinogenesis. 2007 Jul;28(7):1533-42.
23. Int J Cancer. 2008 Jul 1;123(1):41-50.
24. Carcinogenesis. 2007 Jul;28(7):1533-42.
25. Prostate Cancer Res. 2005 May 15;65(10):4448-57.
26. Carcinogenesis. 2007 Jul;28(7):1533-42.
27. Oncogene. 2006 Feb 16;25(7):1053-69.
28. Bioorg Med Chem. 2004 Nov 1;12(21):5677-87.
29. Bio Drugs. 2001;15(7):465-89.
30. Life Sci. 1996;58(18):1591-600.
31. Biochem Pharmacol. 1994 Aug 17;48(4):753-9.
32. J Appl Toxicol. 1992 Dec;12(6):439-42.
33. J Appl Toxicol. 1990 Aug;10(4):275-9.
34. Biotechnol Ther. 1993;4(3-4):263-70.
35. Planta Med. 1989 Oct;55(5):417-9.
36. Food Chem Toxicol. 2008 Jul;46(7):2422-8.
37. Burns. 2007 Nov;33(7):908-16.
38. Indian J Med Res. 2006 Nov;124(5):491-504.
39. Indian J Biochem Biophys. 2006 Oct;43(5):306-11.
40. Planta Med. 1989 Oct;55(5):417-9.
41. Cancer Lett. 1999 Dec 1;147(1-2):77-84.
42. Phytomedicine. 2000 Mar;7(1):21-4.
43. Hepatology. 1996 Apr;23(4):749-54.
44. Life Sci. 1996;58(18):1591-600.
45. Tokai J Exp Clin Med. 1990 May;15(2-3):123-7.
46. J Hepatol. 1989 Jul;9(1):105-13.
47. Scand J Gastroenterol. 1982 Jun;17(4):517-21.
48. Med Klin. 1978 Jul 14;73(28-29):1060-5.
49. Tohoku J Exp Med. 2007 Nov;213(3):261-8.
50. Mol Biotechnol. 2007 Sep;37(1):58-61.
51. Life Extension-sponsored study #1.
52. Phytother Res. 2004 Dec;18(12):957-62.
53. Eur Ann Allergy Clin Immunol. 2007 Feb;39(2):45-50.
54. Anticancer Res. 2004 Mar-Apr;24(2B):563-9.
55. Toxicol Lett. 2000 Mar 15;112-113:499-505.
56. J Pharm Pharmacol. 1997 Jan;49(1):105-7.
57. Antioxid Redox Signal. 2008 Mar;10(3):511-45.
58. Asia Pac J Clin Nutr. 2008;17 Suppl 1:265-8.
59. J Alzheimer’s Dis. 2004 Aug;6(4):367-7.
60. Chin Med. 2008 Sep 17;3:11.
61. Dig Dis Sci. 2005 Nov;50(11):2191-3.
62. Biochem Pharmacol. 2008 Feb 15;75(4):787-809.
63. J Endotoxin Res. 2007;13(1):15-23.
64. Prostaglandins Leukot Essent Fatty Acids. 1995 Apr;52(4):223-7.
65. Mol Cancer Ther. 2006 May;5(5):1371-82.
66. J Ethnopharmacol. 1993 Mar;38(2-3):113-9.
67. Mol Nutr Food Res. 2008 Sep;52(9):1031-9.
68. Eur J Pharmacol. 2007 Dec 22;577(1-3):183-91.
69. Spice India. 2006 Sept;19(9):11-5.
70. A novel bioenhanced preparation of curcuminoids. Study submitted for publication, 2007.
71. J Am Coll Nutr. 2004 Jun;23(3):197-204.
72. JAMA. 2003 Aug 27; 290(8):1030-1.
73. Am J Clin Nutr. 2005 Mar;81(3):611-4.
74. Free Radic Biol Med. 2004;37:1351–1359.
75. Am J Clin Nutr. 2005 Mar;81(3):611-4
76. Am J Clin Nutr. 2007 Mar;85(3):709-17.
77. Hypertension. 2005a Aug;46(2):398-405.
78. Clin Dev Immunol. 2005;12:11–17.
79. J Med Food. 2005 Spring;8(1):8-13.
80. J Agric food Chem. 2005 May 4;53(9):3403-7.
81. Nutr Neurosci. 2002 Dec;5(6):427-31.
82. J Alzheimers Dis. 2006 Mar;9(1):35-42.
83. J Neurosci. 1999 Sep 15;19(18):8114-21.
84. Neurobiol Aging. 2005 Dec;26 Suppl 1:128-32.
85. Mutat Res. 2003 Feb 5;535(1):103-15.
86. Neurobiol Aging. 2006 Feb;27(2):344-50.
87. Nitric Oxide. 2006 Nov;15(3):259-63.
88. Nitric Oxide. 2006 Sep;15(2):93-102.
89. Cardiovasc Res. 2007 Jan 15;73(2):414-23.
90. Life Sci. 2006 Jul 10;79(7):641-5.
91. J Agric Food Chem. 2004 Jul 28;52(15):4713-9.
92. New Larousse Encyclopedia of Mythology. London: Hamly; 1983.
93. Atherosclerosis. 2006 Aug;187(2):363-71.
94. J Agric Food Chem. 2002 Aug 14;50(17):4791-5.
95. J Agric Food Chem. 2000 Oct;48(10):4581-9
96. J Agric Food Chem. 2005 (53):6126-32.
97. Zhonghua Yu Fang Yi Xue Za Zhi. 2005 Mar;39(2):80-3.
98. Food Chem Toxicol. 2006 Jul;44(7):984-93.
99. Eur J Nutr. 2003 Jan;42(1):18-28
100. Biochem Pharm. 2002, 64;393-404.
101. Toxicol Appl Pharm. 2001 Jul 15;174(2):146-52.
102. J Natl Cancer Inst. 1997 May 21;89(10):718-23.
103. Cancer Detect Prevent. 2004;28:72-9.
104. Carcinogenesis. 2002 Apr;23(4):581-6.
105. Mol Cancer Ther. 2003 Oct;2(10):1045-52.
106. Carcinogenesis. 1998 Oct;19(10):1821-7.
107. Carcinogenesis 1995 Sep;16(9):2057-62.
108. Arch Pharm Res. 2008 Oct;31(10):1303-11.
109. Neuroimmunomodulation. 2006;13(3):179-86.
110. Eur J Cardiovasc Prev Rehabil. 2005;12:596-600.
111. Biochem J. 2005;386:471-8.
112. J Cardiovasc Pharmacol. 2005 Oct;46(4):445-51.
113. Int J Dev Neurosci. 2005 Oct;23(6):501-7.
114. Clin Interv Aging. 2008;3(2):331-9.
115. Altern Med Rev. 2001 Apr;6(2):207-9
116. Biosci Biotechnol Biochem. 2007 Sep;71(9):2223-32.
117. Indian J Exp Biol. 1999 Feb;37(2):124-30.
118. Biol Pharm Bull. 2002 Sep;25(9):1197-202.
119. Immunology. 2005 Jul;115(3):375-87.
120. Life Sci. 2007 Nov 30;81(23-24):1602-14
121. Pancreas. 2007 Nov;35(4):e1-9.
122. Exp Biol Med. 2004 Mar;229(3):247-54.
123. Carcinogenesis. 1995 Sep;16(9):2057-62.
124. J Agric Food Chem. 2004 Aug 11;52(16):5004-10.
125. Food Chem Toxicol. 2001 Feb;39(2):109-17.
126. Biofactors. 2000;13(1-4):161-6.
127. J Food Prot. 2000 Oct;63(10):1359-68.
128. Carcinogenesis. 1998 Oct;19(10):1821-7.
129. J Nutr. 1996 May;126(5):1475-80.
130. Inf amm Res. 1996 Nov;45(11):546-9
131. Altern Med Rev. 2000 Aug;5(4):372-5.
132. Chem Res Toxicol. 2003 Sep;16(9):1155-61.
133. Addict Biol. 2002 Jul;7(3):307-14.
134. Arch Biochem Biophys. 1999 Feb 1;362(1):79-86.
135. Free Radic Biol Med. 2003 Mar 15;34(6):648-62.
136. J Periodontol. 1993 Jul;64(7):630-6.
137. In Vivo. 2004 Jan-Feb;18(1):55-62.
138. Am J Clin Nutr. 1999 Dec;70(6):1040-5.
139. Curr Drug Metab. 2003 Jun;4(3):241-8.
140. Arch Pharm Res. 2000 Dec;23(6):605-12.
141. Carcinogenesis. 2000 Jan;21(1):63-7.
142. Proc Soc Exp Biol Med. 1999 Apr;220(4):239-43.
143. J Cell Biochem Suppl. 1997;27:68-75.
144. Chem Biol Interact. 1995 Dec 22;98(3):283-301.
145. Life Sci. 1998;63(16):1397-403.
146. Arch Intern Med. 2003 Jun 23;163(12):1448-53.
147. J Gastroenterol. 2000;35 Suppl 12:1-6. Review.
148. Cell Immunol. 2005 Sep;237(1):7-16.
149. J Environ Pathol Toxicol Oncol. 1999;18(3):147-58.
150. Cell Mol Life Sci. 2003 Sep;60(9):1779-92.
151. Altern Med Rev. 2001 Apr;6(2):141-66.
152. Clin Physiol Funct Imaging. 2002 Nov;22(6):375-8.
153. Presse Med. 1986 Sep 25;15(31):1550-3.
154. Brain Res. 1997 May 2;755(2):347-50.
155. Clin Chim Acta. 2004 Feb;340(1-2):153-62.
156. Pharmacopsychiatry. 2003 Jun;36 Suppl 1:S89-94.
157. Ann N Y Acad Sci. 2005 Nov;1056:474-85.
158. Rev Prat. 2000 Jun 1;50(11):1195-8.
159. Altern Ther Health Med. 2001 Sep-Oct;7(5):70-86, 88-90.
160. Int J Microcirc Clin Exp. 1997 Mar-Apr;17(2):61-6.
161. J Ethnopharmacol. 1996 Mar;50(3):131-9.
162. Pharmacol Res. 2002 Dec;46(6):565-8.
163. Phlebologie. 1991 Jul-Oct;44(3):779-86.
164. Phlebologie. 1991 Apr-Jun;44(2):509-16.
165. Acta Neurochir Suppl. 2000;76:87-90.
166. Presse Med. 1986 Sep 25;15(31):1575-6.
167. Pharmacopsychiatry. 1996 Mar;29(2):47-56.
168. Adv Ther. 1998 Jan-Feb;15(1):54-65.
169. Antioxid Redox Signal. 2007 Oct;9(10):1659-75.
170. Free Radic Biol Med. 1999; Sep;27(5-6):596-604.
171. Mol Biother. 1991 Jun;3(2):103-7.
172. Carcinogenesis. 1993 Aug;14(8):1627-31.
173. Carcinogenesis. 1992 Oct;13(10):1847-51.
174. J R Coll Physicians Lond. 1994 Jan-Feb;28(1):39-45.
175. Pharmacotherapy. 1993 Jul-Aug;13(4):406-7.
176. J Cardiovasc Pharmacol. 1998 Jun;31(6):904-8.
177. Nippon Yakurigaku Zasshi. 1997 Oct;110 Suppl 1:93P-97P.
178. Clin Exp Pharmacol Physiol. 1997 Mar-Apr;24(3-4):235-42.
179. Exp Gerontol. 1997 Jan-Apr;32(1-2):149-60.
180. Nutr Cancer. 1999;34(1):42-8.
181. Jpn J Pharmacol. 1998 Oct;78(2):199-207.
182. J Am Coll Nutr. 2001 Jun;20(3):225-31.
183. Planta Med. 2001 Feb;67(1):13-8.
184. Antimicrob Agents Chemother. 1977 Apr;11(4):743-9.
185. Am J Hypertens. 2007 Aug;20(8):866-74.
186. Am J Physiol Heart Circ Physiol. 2006 Nov;291(5):H2431-8.
187. Clin Nutr. 2004 Oct;23(5):1199-208.
188. Nutr Res. 1996, 16/4 (673-681).
189. Biochem Med Metab Biol. 1990 Apr;43(2):83-92.
190. Chest. 2004 May;125(5 Suppl):149S-150S.
191. J Med Sci (Israel). 1995;31(2-3):101-5.
192. Anticancer Res. 1995 May-Jun; 15(3):805-10.
193. Life Sci. 1994;54(18):1299-303.
194. Toxicology. 1992 Sep;74(2-3):209-22.
195. Altern Med Rev. 2002 Aug;7(4):336-9.
196. Integr Cancer Ther. 2003 Jun;2(2):139-44.
197. Postepy Hig Med Dosw (Online). 2008 Sep 5;62:451-62.
198. Biochemical Pharmacology (United Kingdom). 1991;41(10):1471-77.
199. Cancer Lett. 1990 Jan;49(1):51-7.
200. Cancer Lett. 1986 Oct;33(1):25-32.
201. Methods Mol Biol. 2004;274:159-71.
202. Mutat Res. 2003 Feb-Mar;523-524:217-23.
203. Cancer Lett. 1996 Nov 29;108(2):247-55.
204. Carcinogenesis. 1989 Jan;10(1):145-9.
205. Mutat Res. 2003 Feb-Mar;523-524:209-16.
206. Chem Res Toxicol. 1995 Jun;8(4):506-14.
207. Int J Food Sci Nutr. 2004 May;55(3):249-56.
208. Free Radic Biol Med. 2004 Apr 15;36(8):1058-67.
209. Platelets. 2001 Jun;12(4):218-27.
210. Eur J Nutr. 2004 Aug;43(4):237-45.
211. BMJ. 2003 Aug 23;327(7412):451.
212. Carcinogenesis. 1995 Feb;16(2):399-404.
213. Nutr Cancer. 1989;12(2):121-6.
214. Cancer Epidemiol Biomarkers Prev. 2004 Jan;13(1):125-31.
215. J Agric Food Chem. 2001 May;49(5):2679-83.
216. Cancer Epidemiol Biomarkers Prev. 2001 May;10(5):501-8.
217. Theor Appl Genet. 2003 Feb;106(4):727-34.
218. Cancer Epidemiol Biomarkers Prev. 2004 Mar;13(3):340-5.
219. J Natl Cancer Inst. 2003 Nov 5;95(21):1578-86.
220. Lipids. 1998 Oct;33(10):981-4.
221. J Nutr. 2003 Mar;133(3):727-32.
222. Exp Biol Med (Maywood). 2002 Nov;227(10):881-5.
223. Cancer Epidemiol Biomarkers Prev. 2001 Aug;10(8):861-8.
224. Nutr Cancer. 1999;33(2):159-64.
225. Am J Epidemiol. 2002 Jun 1;155(11):1023-32.
226. Exp Biol Med (Maywood). 2002 Nov;227(10):881-5.
227. J Natl Cancer Inst. 2002 Mar 6;94(5):391-8.
228. J Nutr. 2008 Jan;138(1):49-53.
229. Arch Biochem Biophys. 2008 Nov 1. [Epub ahead of print]
230. Asia Pac J Clin Nutr. 2007;16 Suppl 1:453-7.
231. Int Angiol. 1993 Mar;12(1):69-72.
232. Drugs. 2003;63(1):71-100.
233. Am J Clin Nutr. 2002 Sep;76(3):560-8.
234. J Nutr. 2003 Jun;133(6):1892-7.
235. J Ocul Pharmacol Ther. 2004 Apr;20(2):107-13.
236. Int J Mol Med. 2006 Mar;17(3):511-5.
237. J Agric Food Chem. 2008 Feb 13;56(3):824-9.
238. Immunopharmacol Immunotoxicol. 2008;30(1):117-34.
239. Int Immunopharmacol. 2008 May;8(5):670-8..
240. Nutr Cancer. 2008;60(1):69-74.
241. J Biochem Mol Toxicol. 2008 Jul;22(4):268-73.
242. Neurosci Lett. 2008 Jun 13;438(1):29-33.
243. Arch Pharm Res. 2008 Nov;31(11):1457-62.
244. Int Angiol. 2003 Sep;22(3):250-62.
245. Actas Urol Esp. 2003 Oct;27(9):732-4.
246. Biol Pharm Bull. 2004 May;27(5):679-83.
247. Clin Chim Acta. 2003 Jan;327(1-2):129-37.
248. Toxicology. 2006 Sep 21;226(2-3):152-60.
249. J Agric Food Chem. 1999 Nov;47(11):4649-52.
250. Biochim Biophys Acta. 1984 Jun 29;799(3):313-7.
251. Blood. 1951 Jun;6(6):552-4.
252. J Lab Clin Med. 1950 Jun;35(6):933-9.
253. Vopr Kurortol Fizioter Lech Fiz Kult. 2000 Mar-Apr;(2):31-4.
254. Farmaco. 2001 Sep;56(9):683-7.
255. Phytomedicine. 2004 Feb;11(2-3):105-13.
256. Zhongguo Zhong Yao Za Zhi. 2007 Oct;32(19):2058-62.
257. BMC Cardiovasc Disord. 2001;1(1):5.
258. Pharmacol Res. 2001 Sep;44(3):183-93.
259. Angiology. 2000 Mar;51(3):197-205.
260. J Fam Pract. 1999 Mar;48(3):171-2.
261. Arch Dermatol. 1998 Nov;134(11):1356-60.
262. Arzneimittelforschung. 1994 Jan;44(1):25-35.
263. Arzneimittelforschung. 1994 Jan;44(1):25-35.
264. Pharmacol Res. 2001 Sep;44(3):183-93.
265. Arzneimittelforschung. 1979;29(4):672-5.
266. Arzneimittelforschung. 1979;29(4):672-5.
267. Toxicol Appl Pharmacol. 1997 Jun;144(2):279-86.
268. Phytother Res. 2008 Sep;22(9):1159-61.
269. Phytomed. 1996. Suppl 1: 50.
270. Planta Med. 2002 Sep;68(9):776-9.
271. Phytomedicine. 2002 Dec;9(8):687-93.
272. Phytother Res. 2001 Feb;15(1):58-61.
273. Br J Nutr. 2007 Sep;98(3):540-9.
274. J Altern Complement Med. 2004 Aug;10(4):667-9.
275. Exp Toxicol Pathol. 2008 Sep;60(6):475-80.
276. Nutr Cancer. 2008;60(2):276-83.
277. Cell Biology and Toxicology, 1996.
278. Mol Nutr Food Res. 2008 Oct;52(10):1147-52.
279. J Pharmacol Exp Ther. 2004 Sep;310(3):926-32.
280. Life Sci. 2004 Dec 31;76(7):775-82.
281. J Agric Food Chem. 2005 Dec 28;53(26):10291-6.
282. Phytomedicine. 2008 Sep;15(9):668-75.
283. J Pharmacol Exp Ther 286: 3, 1998.
284. Phytomedicine 1: 107, 1994.
285. Filoterapia 48: 153,1977.
286. Trends Pharmacol Sci. 2006 Dec;27(12):619-25.
287. Neurosci Lett. 2004 May 6;361(1-3):56-9.
288. Eur J Pharmacol. 2002 Nov 29;455(2-3):101-7.
289. Zhongguo Yao Li Xue Bao. 1999 Feb;20(2):141-5.
290. Zhongguo Yao Li Xue Bao. 1998 Jan;19(1):27-30.
291. Neuroreport. 1996 Dec 20;8(1):97-101.
292. Chem Biol Interact. 2008 Sep 25;175(1-3):396-402.
293. Pharmacol Biochem Behav. 2006 Apr;83(4):603-11.
294. Zhonghua Yi Xue Za Zhi. 2002 Jul 25;82(14):941-4.
295. Zhongguo Yao Li Xue Bao. 1999 Jul;20(7):601-3.
296. Zhongguo Yao Li Xue Bao. 1999 Jun;20(6):486-90.
297. Zhongguo Yao Li Xue Bao. 1995 Sep;16(5):391-5.
298. Crit Rev Food Sci Nutr. 2006;46(2):185-96.
299. Biol Pharm Bull. 2005 Jan;28(1):47-52.
300. Life Sci. 2007 Jan 16;80(6):522-9.
301. Ophthalmology. 2008 Feb;115(2):324-333.e2.
302. Environ Geochem Health. 2007 Dec;29(6):483-9.
303. J Ethnopharmacol. 2001 Oct;77(2-3):203-8.
304. Acupunct Electrother Res. 1995 Aug-Dec;20(3-4):195-229.
305. Acupunct Electrother Res. 1996 Apr-Jun;21(2):133-60.
306. Environ Pollut. 2001;114(1):85-92.
307. J Biotechnol. 1999 Apr 30;70(1-3):33-8.
308. Bull Environ Contam Toxicol. 1999 Feb;62(2):144-51.
309. Biomed Environ Sci. 1991 Sep;4(3):250-61.
310. Radioisotopes. 1979 Aug;28(8):485-8
311. Bull Environ Contam Toxicol. 2003 May;70(5):1036-44.
312. Am J Clin Nutr. 1985 Oct;42(4):618-28.
313. Mycoses. 2003 Apr;46(3-4):132-6. 449-453
314. Pharm Pharmacol. 1999 Aug;51(8):971-4.
315. Microbios. 1998;93(374):43-54.
316. J Appl Bacteriol. 1988 Apr;64(4):293-7.
317. J Nutr. 2001 Mar;131(3s):1010S-5S.
318. J Cardiovasc Pharmacol. 1998 Jun;31(6):904-8.
319. Cancer Immunol Immunother. 1993 Oct;37(5):316-22.
320. Prev Med. 2004 Nov;39(5):985-91.
321. J Nutr. 2001 Mar;131(3s):980S-4S.
322. J Nutr. 2000 Nov;130(11):2662-5.
323. Hiroshima J Med Sci. 2006 Jun;55(2):59-64.
324. Eur J Pharmacol. 2007 Apr 30;561(1-3):32-8.
325. Phytother Res. 2007 Jul;21(7):629-40.
326. J Nutr. 2007 Oct;137(10):2264-9. Review.
327. Cancer Chemother Pharmacol. 2008 Aug 2. [Epub ahead of print]
328. Iran J Allergy Asthma Immunol. 2008 Sep;7(3):133-41.
329. Mol Biother. 1991 Jun;3(2):103-7.
330. Free Radic Res. 2008 Dec 29:1-10.
331. Br J Nutr. 2008 Nov 14:1-6.
332. Biochem Pharmacol. 2004 Nov 15;68(10):1939-46.
333. Int Immunopharmacol. 2008 Dec 2. [Epub ahead of print]
334. J Neuroimmunol. 2008 Dec 15;205(1-2):142-7.
335. Mol Cell Endocrinol. 2008 Jun 11;287(1-2):57-64.
336. Inflamm Res. 2007 May;56(5):210-5.
337. Zhongguo Zhong Yao Za Zhi. 2007 Oct;32(19):2058-62.
338. Biochem Biophys Res Commun. 2009 Jan 10. [Epub ahead of print]
339. Am J Clin Nutr. 2008 Oct;88(4):1018-25.
340. Atherosclerosis. 2008 Aug 14. [Epub ahead of print]
341. Acta Neurobiol Exp (Wars). 2008;68(4):463-76.
342. J Nutr. 2009 Jan;139(1):101-5.
343. J Cell Biochem. 2009 Jan 1;106(1):73-82.
344. Chemotherapy. 2009;55(1):6-10.
345. Arch Pharm Res. 2008 Oct;31(10):1281-5.
346. Prostate. 2008 Dec 1;68(16):1773-89.
347. J Agric Food Chem. 2003 Oct 22;51(22):6618-22.
348. Food Chem Toxicol. 2008 Jul;46 Suppl 7:S11-20.
349. Food Chem Toxicol. 2008 Jul;46 Suppl 7:S1-S10.
350. Int J Toxicol. 2008 Jan-Feb;27(1):65-80.
351. Food Chem Toxicol. 2003 Mar;41(3):359-74.
352. J Toxicol Sci. 2002 Dec;27 Suppl 1:1-8. Japanese.
353. Metabolism. 2004 Jan;53(1):73-6.
354. Braz J Med Biol Res. 1986;19(6):771-4.



The information herein is not intended to replace the medical advice of your physician. You are advised to consult with your physician with regards to matters relating to your health, and in particular regarding matters that may require diagnosis or medical attention. DO NOT stop taking medications without first consulting with your physician. 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.

Every effort has been made to ensure that the information provided herein is accurate, up-to-date, and complete, but no guarantee is made to that effect. This information has been compiled for use by healthcare practitioners and consumers in the United States. Heart 2 Heart of America does not endorse drugs, diagnose patients or recommend therapy. This informational resource is designed to assist licensed healthcare practitioners in caring for their patients and/ or to serve consumers viewing this service as a supplement to, and not a substitute for, the expertise, skill, knowledge and judgment of healthcare practitioners. Heart 2 Heart of America does not assume any responsibility for any aspect of healthcare administered with the aid of information Heart 2 Heart of America compiles. The information contained herein is not intended to cover all possible uses, directions, precautions, warnings, drug interactions, allergic reactions, or adverse effects. If you have questions, check with your doctor, nurse or pharmacist.