Joint Health and Flexibility Kit
Earn $2.80 ma Cashback
As we get older, the effect that aging has on our bodies becomes more obvious. One of the most noticeable signs of aging occurs in joint health. As we age, the wellbeing of our joints begins to deteriorate, causing joint discomfort, limited mobility and overall poor joint health. For this reason, it is important to combat the effects that aging places on our joints. To help with the fight for optimal joint health, we have combined three products (Prime™ Joint Support Formula by Isotonix, Curcumin Extreme™ and Heart Health™ Omega III Fish Oil with Vitamin E) to create the Joint Health and Flexibility Kit.
The Joint Health and Flexibility Kit is an ideal combination of products, designed to support healthy and flexible joints. This grouping of products supports joint health, offers temporary inflammation relief, and promotes tissue hydration and lubrication. In addition, the Joint Health and Flexibility Kit offers 22% in savings from the individual suggested retail prices of the products.
The purpose of the Joint Health and Flexibility Kit is to help individuals maintain their joint health while contributing to overall mobility and flexibility. This kit contains Prime™ Joint Support Formula which contains glucosamine (naturally produced by the body), an ingredient concentrated in joint cartilage, which has also been scientifically proven to support healthy joint function. Prime™ Joint Support Formula also contains the powerful antioxidant Pycnogenol®, which in connection with Curcumin Extreme promotes the reduction of inflammation associated with normal aging.
The final piece of the Joint Health and Flexibility Kit is Heart Health™ Essential Omega III with Vitamin E. Heart Health™ Essential Omega III matches well with Prime Joint Support Formula and Curcumin Extreme, as omega-3 fatty acids have been shown to support healthy joint lubrication.
- Save $38.45 compared to purchasing these products separately - a 22% savings!
- Supports relief from temporary inflammation associated with the normal aging process and daily activity
- Helps maintain healthy joint fluidity and flexibility
- Promotes normal cartilage synthesis and regeneration
- Promotes optimal joint health
- Helps maintain joint comfort
- Supports normal, healthy levels of COX-2 and 5-LOX
Prime™ Joint Support Formula by Isotonix®:
Glucosamine (HCl) 1000 mg
Glucosamine is a molecule that is naturally synthesized in the body from glucose and the amino acid glutamine. Glucosamine is an important constituent of glycosaminoglycans in cartilage matrix and synovial fluid. As our bodies age, we are less able to produce glucosamine, resulting in cartilage that is less flexible and weak. Although the mechanism is currently unclear, studies have shown that glucosamine supplementation can support normal, healthy cartilage cell production to help maintain overall joint health.
Pine Bark Extract (Pycnogenol®) 25 mg
Pycnogenol is a water-soluble, flavonoid complex with powerful benefits. Pycnogenol, similar to the proanthocyanins found in grape seeds, is extracted from the bark of the French Maritime Pine tree. Numerous studies have examined the anti-inflammatory properties of Pycnogenol.
The body’s inflammatory response is a natural process. It is an essential component of the body’s defense system, and can be triggered from numerous internal and external factors. Pycnogenol has been shown help maintain the body’s natural defenses by inhibiting over active inflammatory responses associated with the normal aging process. Research has shown that Pycnogenol may inhibit the activation of NF-kappa B and AP-1, both of which are proinflammatory mediators. Pycnogenol supplementation can also promote normal COX-2 and 5-LOX gene expression, and support healthy leukotriene biosynthesis. In addition, studies have shown the ability of Pycnogenol to cross-link collagen fibers and strengthen connective tissue proteins.
To learn more about the relationship between Pycnogenol and joint health, follow the links below to read the full text studies.
Hyaluronic Acid (Sodium Hyaluronate) 25 mg
Hyaluronic acid plays an important role in tissue hydration, lubrication and cellular function. Although it is produced naturally by the body, the level of hyaluronic acid diminishes with age, contributing to joint discomfort. It is a key component of cartilage, and is important for skin, joint and eye health. Hyaluronic acid has been shown to help maintain strong, healthy cartilage. It may also enhance synovial fluid production and promote normal healing.
Curcumin (BCM-95®) 400 mg
Scientists have long been aware of the wide array of health benefits from the Indian spice turmeric, which is a source of the active phytochemical curcumin. Until now, curcumin has been known to have poor bioavailability, requiring high doses to promote health. BCM-95® delivers significantly more pharmacologically bioactive curcumin into the blood than other curcumin sources. This new delivery system allows for a variety of health supporting results.
How is this possible? Traditional 95% extract focuses strictly on one part of the Turmeric rhizome. This bioactive substance of Turmeric (Curcuma Longa) contains “Curcuminoids” and Curcumin is the most important molecule. Research has shown its tremendous health benefit. Even though Curcumin is the most important molecule, the bioavailability of the regular Turmeric 95% extracts sold on the market is not very good in terms of uptake or sustainability in the blood stream. There are other essential components present in Turmeric Rhizome which have been neglected during the traditional method of manufacturing of Turmeric 95% Extract. BCM-95® represents the natural spectrum of turmeric rhizome. It is 100 percent natural and has been proven to provide optimal bioavailability for synergistic effect. This new method of manufacture offers tremendous value in terms of bioavailability.
Antioxidants have received increased attention, and it’s important to know what nutrients are antioxidants and information about them. One such nutrient is Curcumin. Curcumin is a natural extract from the spice turmeric. Turmeric is derived from the plant Curcuma Longa, a member of the ginger family.
Curcumin is employed mostly as an antioxidant; though it was traditionally used to promote stomach and joint comfort. The immune-balancing activity of curcumin has been demonstrated through multiple mechanisms to support normal COX-2 and NF-KappaB levels in the body.
The neuroprotective properties of curcumin are among the most studied. Curcumin has been designated as a strong candidate for the promotion of neurological health and cognitive function. Curcumin can cross the blood-brain barrier and support the normal uptake of amyloid-beta in the brain. This supports the brain's memory and learning abilities as we age. Another neuroprotective property of curcumin is its ability to promote normal levels of glutathione, superoxide dismutase and catalase in the brain. This can help to maintain the health of neurological tissues.
Curcumin supports the normal production of Phase II liver detoxification enzymes including glutathione synthase, heme-oxygenase and catalase. The liver plays several roles in detoxification: it filters the blood to remove large toxins, synthesizes and secretes bile full of cholesterol and other fat-soluble toxins, and enzymatically disassembles unwanted chemicals. This enzymatic process usually occurs in two steps referred to as phase I and phase II. They promote the body’s natural enzyme antioxidant defense systems and function as a powerful indirect antioxidant. These enzymes promote the body’s normal metabolism of harmful chemicals, such as heavy metals, toxins and pollutants into less reactive molecules. Curcumin has also been shown to promote normal hepatic tissue repair.
Broccoli Seed Extract (6% Sulphoraphane Glucosinolates) 167 mg
The health benefits and protective properties of broccoli and other cruciferous vegetables have been well documented over the past 25 years. Broccoli seed extract is a powerful source of sulphoraphane glucosinolates. Sulforaphanes support the normal production of Phase II liver detoxification enzymes including glutathione synthase, heme-oxygenase and catalase. Sulforaphanes promote the body’s natural enzyme antioxidant defense systems and function as a powerful indirect antioxidant. Sulphoraphanes work to support gene transcription, which is the process by which genetic information is copied from DNA to RNA, resulting in a specific protein formation. Conclusively, sulphoraphanes work to support the body’s natural defense systems and to maintain elevated levels of glutathione.
Glutathione is the master antioxidant of the body. It is an important chemical that acts as a powerful antioxidant to preserve and protect the brain and other body tissues by protecting them from the damage of free radicals. It also acts to recycle vitamin C and E, which also reduce free radicals. Since glutathione cannot be absorbed intact orally due to gastrointestinal degradation, sulphoraphane supplementation may be the most effective way to increase endogenous glutathione concentration.
Selenium (Selenomethionine) 100 mcg
Selenium is a required cofactor for selenoproteins such as glutathione peroxidase. Selenomethionine is incorporated directly into proteins because selenomethionine cannot be distinguished from methionine during the translation of mRNA into protein. This serves as a storage form of selenium and is liberated upon protein catabolism. Selenium accumulates in the prostate, promoting the health of the prostate. Selenium supports immune function by promoting normal growth and development of T helper cells.
Heart Health™ Essential Omega III Fish Oil with Vitamin E:
Fish Body Oils 3000 mg [EPA† 900 mg and DHA† 600 mg]
Fish oils or marine oils are lipids (fats) found in fish, particularly cold water fish like herring, kipper, mackerel, menhaden, pilchard, salmon, sardine and trout, and phytoplankton. The sources of fish oil in Heart Health™ Omega III Fish Oil are sardines and anchovies, tested by the manufacturer and an independent testing company to be virtually free of mercury lead, PCB and other heavy metals. Fish oils are rich sources of omega-3 long-chain polyunsaturated fatty acids. EPA (eicosapentaenoic acid) and DHA (docosahexanenoic acid) are the two most studied fish oils. DHA is a necessary component of the phospholipids in human cellular membranes, especially those found in the brain and retina. Clinical studies have shown omega-3 fatty acids to help maintain healthy triglyceride levels. A strong correlation has also been shown between fish oil consumption and the ability to maintain healthy levels of C-reactive protein. Fish oils are also important in the maintenance of normal blood flow, as they support normal fibrinogen levels (coagulation or blood clotting), which contributes to normal platelet activity.*
EPA and DHA have several mechanisms of action to help maintain normal triglyceride and cholesterol levels, help maintain normal blood flow and pressure, and support normal platelet activity. EPA and DHA help maintain normal triglyceride levels by promoting normal lipogenesis and supporting normal fatty acid oxidation in the liver. EPA and DHA promote the normal transcription of genes coding for lipogenesis enzymes and promote the normal transportation of the regulatory enzymes of fatty acid oxidation. Activating PPAR (peroxisome proliferator-activated receptor) - alpha, helps to support normal fatty acid oxidation. The promotion of normal lipogenesis is done through down-regulation of SREBP (sterol regulatory element binding protein) -1c messenger RNA.*
EPA is the precursor to series-3 prostaglandins (PG), the series-3 thrombaxanes (TX) and the series-5 leukotrienes (LT). More specifically, EPA is a precursor to eicosanoids (TXA3 and LTB5), which promote normal platelet activity and promote normal vasodilation. These effects demonstrate EPA’s potential ability to help maintain normal blood pressure and support normal blood clotting. Fish oils inhibit the arachidonic acid synthesis of thromboxane A2, which help to promote normal platelet activity and vasodilation. Fish oil may also contribute to the normal production of prostacyclin, a prostaglandin that promotes normal vasodilation and supports normal platelet activity.*
Omega-3 fatty acids compete metabolically with omega-6 fatty acids, found in higher amounts in typical western diets. Omega-6 fatty acids may inhibit the incorporation of omega-3 fatty acids into tissue lipids. Omega-3 fatty acids may inhibit the conversion of many omega-6 fatty acids into arachidonic acid. Consumption of omega-3 fatty acids DHA and EPA, a corresponding increase of these fatty acids appears to occur in cell membranes and circulatory lipids along with a simulataneous reduction in omega-6 fatty acids.*
Vitamin E (d-alpha tocopherol) 23 IU
The most valuable sources of dietary vitamin E include vegetable oils, margarine, nuts, seeds, avocados and wheat germ. Safflower oil contains large amounts of vitamin E (about two thirds of the RDA in ¼ cup), and there are trace amounts in corn oil and soybean oil. Vitamin E is actually a family of related compounds called tocopherols and tocotrienols. Vitamin E is available in a natural or synthetic form. In most cases, the natural and synthetic forms are identical except the natural form of vitamin E is better absorbed and retained in the body. The natural form of alpha-tocopherol is known as "d-alpha tocopherol." The synthetic "dl-" form is the most common form found in dietary supplements. For those individuals watching their dietary fat consumption, which is relatively common in the world of dieting, vitamin E intake is likely to be low, due to a reduced intake of foods with high fat content.
The main health benefit of supplemental vitamin E comes from its immune-boosting antioxidant activity. It supports a healthy cardiovascular system. Vitamin E is one of the most powerful fat-soluble antioxidants in the body. In turn, vitamin E protects cell membranes from free radical. Vitamin E is commonly added to fish oil supplements to provide antioxidant protection of DHA and EPA.*
What makes these three products ideal for joint health and flexibility?
Prime Joint Support Formula by Isotonix® contains glucosamine, naturally produced by the body and a key component of cartilage. An aminomonosaccharide (a combination of the amino acid — glutamine and a sugar — glucose), glucosamine is concentrated in joint cartilage, and has been scientifically proven to support healthy joint function and promote the normal production of synovial fluid, which lubricates your joints and regenerates cartilage. Heart Health™ Essential Omega III pairs well with Prime Joint Support Formula, as omega III fatty acids have been shown to support healthy joint lubrication. Like Pycnogenol® in Prime Joint Support Formula, Curcumin Extreme can promote the reduction of inflammation associated with the normal aging process.
How often should I take these three products?
This each product is most effective when taken daily.
Prime™ Joint Support Formula by Isotonix®:
- Belcaro, G., et al. Variations in C-reactive protein, plasma free radicals and fibrinogen values in patients with osteoarthritis treated with Pycnogenol®. Redox Report. 13(6): 271-276, 2008.
- Blewis, M., et al. A model of synovial fluid lubricant composition in normal and injured joints. European Cells and Materials. 13: 26-39, 2007.
- Braham, R., et al. The effect of glucosamine supplementation on people experiencing regular knee pain. British Journal of Sports Medicine. 37(1): 45-49, 2003.
- Canali, R., et al. The anti-inflammatory pharmacology of Pycnogenol® in humans involves COX-2 and 5-LOX mRNA expression in leukocytes. International Immunopharmacology. 9(10): 1145-1149, 2009.
- Chang, X., et al. Inhibition of antithrombin by hyaluronic acid may be involved in the pathogenesis of rheumatoid arthritis. Arthritis Research and Therapy. 7(2): R268-R273, 2005.
- Chou, M., et al. Effects of chondroitin and glucosamine sulfate in a dietary bar formulation on inflammation, interleukin-1beta, matrix metalloprotease-9, and cartilage damage in arthritis. Experimental Biology and Medicine. 230(4): 255-262, 2005.
- Cisár, P., et al. Effect of pine bark extract (Pycnogenol®) on symptoms of knee osteoarthritis. Phytotherapy Research. 22: 1087-1092, 2008.
- Elliott, A., et al. Serum hyaluronan levels and radiographic knee and hip osteoarthritis in African Americans and Caucasians in the Johnston County Osteoarthritis Project. Arthritis and Rheumatism. 52(1): 105-111, 2005.
- Farid, R., et al. Pycnogenol® supplementation reduces pain and stiffness and improves physical function in adults with knee osteoarthritis. Nutrition Research. 27: 692-697, 2007.
- Gaby, A. Natural treatments for osteoarthritis. Alternative Medicine Review. 4(5): 330-341, 1999.
- Gouze, J., et al. Exogenous glucosamine globally protects chondrocytes from the arthritogenic effects of IL-1beta. Arthritis Research and Therapy. 8(6): R173
- Grimm, T., et al. Inhibition of NF-kappaB activation and MMP-9 secretion by plasma of human volunteers after ingestion of maritime pine bark extract (Pycnogenol®). Journal of Inflammation. 3: 1-15, 2006.
- Hua, J., et al. Inhibitory actions of glucosamine, a therapeutic agent for osteoarthritis, on the functions of neutrophils. Journal of Leukocyte Biology. 71(4): 632-640, 2002.
- James, C. and Uhl, T. A review of articular cartilage pathology and the use of glucosamine sulfate. Journal of Athletic Training. 36(4): 413-419, 2001.
- Julovi, S., et al. Inhibition of interleukin-1beta-stimulated production of matrix metalloproteinases by hyaluronan via CD44 in human articular cartilage. Arthritis and Rheumatism. 50(2): 516-525, 2004.
- Laurent, T., et al. Functions of hyaluronan. Annals of the Rheumatic Disease. 54(5): 429-432, 1995.
- Kelly, G. The role of glucosamine sulfate and chondroitin sulfates in the treatment of degenerative joint disease. Alternative Medicine Review. 3(1): 27-39, 1998.
- McDonald, J. and Levick, J. Hyaluronan reduces fluid escape rate from rabbit knee joints disparately from its effect on fluidity. Experimental Physiology. 79(1): 103-106, 1994.
- Nakatani, S., et al. Glucosamine regulates differentiation of a chondrogenic cell line, ATDC5. Biological and Pharmaceutical Bulletin. 30(3): 433-438, 2007.
- Ohno, S., et al. Hyaluronan oligosaccharides induce matrix metalloproteinase 13 via transcriptional activation of NFkappaB and p38 MAP kinase in articular chondrocytes. Journal of Biological Chemistry. 281(26): 17952-17960, 2006.
- Poustie, M., et al. N-butyryl glucosamine increases matrix gene expression by chondrocytes. Journal of Pharmacology and Experimental Therapeutics. 311(2): 610-616, 2004.
- Reginster, J., et al. Current concepts in the therapeutic management of osteoarthritis with glucosamine. Bulletin (Hospital for Joint Disease). 63(1-2): 31-36, 2005.
- Reginster, J., et al. Long-term effects of glucosamine sulphate on osteoarthritis progression: a randomized, placebo-controlled clinical trial. Lancet. 357(9252): 251-256, 2001.
- Richy, F., et al. Structural and symptomatic efficacy of glucosamine and chondroitin in knee osteoarthritis: a comprehensive meta-analysis. Archives of Internal Medicine. 163(13): 1514-1522, 2003.
- Santangelo, K., et al. Effects of hyaluronan treatment on lipopolysaccharide-challenged fibroblast-like synovial cells. Arthritis Research and Therapy. 9(1): R1, 2007.
- Sasaki, A., et al. Hyaluronate inhibits the interleukin-1beta-induced expression of matrix metalloproteinase (MMP)-1 and MMP-3 in human synovial cells. The Tohoku Journal of Experimental Medicine. 204(2): 99-107, 2004.
- Schäfer, A., et al. Inhibition of COX-1 and COX-2 activity by plasma of human volunteers after ingestion of French maritime pine bark extract (Pycnogenol®). Biomedicine and Pharmacotherapy. 60: 5-9, 2006.
- Araujo, C. and Leon, L. Biological activities of Curcuma longa L. Memorias do Instituto Oswaldo Cruz. 96(5): 723-728, 2001.
- Bhattacharyya, S., et al. Curcumin prevents tumor-induced T cell apoptosis through Stat-5a-mediated Bcl-2 induction. Journal of Biological Chemistry. 282(22): 15954-15964.
- Biswas, S., et al. Curcumin induces glutathione biosynthesis and inhibits NF-kappaB activation and interleukin-8 release in alveolar epithelial cells: mechanism of free radical scavenging activity. Antioxidants and Redox Signaling. 7(1-2): 32-41, 2005.
- Cheng, Y., et al. Effects of curcumin on peroxisome proliferator-activated receptor gamma expression and nuclear translocation/redistribution in culture-activated rat hepatic stellate cells. Chinese Medical Journal. 120(9): 794-801, 2007.
- Churchill, M., et al. Inhibition of intestinal tumors by curcumin is associated with changes in the intestinal immune cell profile. Journal of Surgical Research. 89(2): 169-175, 2000.
- Cornblatt, B., et al. Preclinical and clinical evaluation of sulforaphane for chemoprevention in the breast. 28(7): 1485-1490, 2007.
- Dairam, A., et al. Curcuminoids, curcumin, and demethoxycurcumin reduce lead-induced memory deficits in male Wistar rats. Journal of Agricultural and Food Chemistry. 55(3): 1039-1044, 2007.
- Dickinson, D., et al. Curcumin alters EpRE and AP-1 binding complexes and elevates glutamate-cysteine ligase gene expression. FASEB. 17(3): 473-475, 2003.
- Fahey, J., et al. Sulforaphane inhibits extracellular, intracellular, and antibiotic-resistant strains of Helicobacter pylori and prevents benzo[a]pyrene-induced stomach tumors. Proceedings of the National Academy of Sciences of the United States of America. 99(11): 7610-7615, 2002.
- Farombi, E., et al. Curcumin attenuates dimethylnitrosamine-induced liver injury in rats through Nrf2-mediated induction of heme oxygenase-1. Food and Chemical Toxicology. 46(4): 1279-1287, 2008.
- Funk, J., et al. Turmeric extracts containing curcuminoids prevent experimental rheumatoid arthritis. Journal of Natural Products. 69(3): 351-355, 2006.
- Gao, X. and Talalay, P. Induction of phase 2 genes by sulforaphane protects retinal pigment epithelial cells against photooxidative damage. Proceedings of the National Academy of Sciences of the United States of America. 101(28): 10446-10451, 2004.
- Garcia-Alloza, M., et al. Curcumin labels amyloid pathology in vivo, disrupts existing plaques, and partially restores distorted neurites in an Alzheimer mouse model. Journal of Neurochemistry. 102(4): 1095-1104, 2007.
- Heiss E, Herhaus C, Klimo K, et al. Nuclear factor kappa B is a molecular target for sulforaphane-mediated anti-inflammatory mechanisms. J Biol Chem 2001;276:32008-15.
- Higdon, J., et al. Cruciferous vegetables and human cancer risk: epidemiologic evidence and mechanistic basis. Pharmacological Research. 55(3): 224-236, 2007.
- Howells, L., et al. Comparison of oxaliplatin- and curcumin-mediated antiproliferative effects in colorectal cell lines. International Journal of Cancer. 121(1): 175-183, 2007.
- Jagetia, G. and Aggarwal, B. "Spicing up" of the immune system by curcumin. Journal of Clinical Immunology. 27(1): 19-35, 2007.
- Johnson, J., et al. Curcumin for chemoprevention of colon cancer. Cancer Letters. 255(2): 170-181, 2007.
- Juge, N., et al. Molecular basis for chemoprevention by sulforaphane: a comprehensive review. Cellular and Molecular Life Sciences. 64(9): 1105-1127, 2007.
- Kaur, G., et al. Inhibition of oxidative stress and cytokine activity by curcumin in amelioration of endotoxin-induced experimental hepatoxicity in rodents. Clinical and Experimental Immunology. 145(2): 313-321, 2006.
- Kim, G., et al. Curcumin inhibits immunostimulatory function of dendritic cells: MAPKs and translocation of NF-kappa B as potential targets. Journal of Immunology. 174(12): 8116-8124, 2005.
- Kuptniratsaikul V, Thanakhumtorn S, Chinswangwatanakul P, et al. Efficacy and safety of Curcuma domestica extracts in patients with knee osteoarthritis. J Altern Complement Med 2009;15:891-7.
- Kurup, V., et al. Immune response modulation by curcumin in a latex allergy model. Clinical and Molecular Allergy. 5: 1, 2007.
- Lim, G., et al. The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse. Journal of Neuroscience. 21(21): 8370-8377, 2001.
- Lin, J. Molecular targets of curcumin. Advances in Experimental Medicine and Biology. 595: 227-243, 2007.
- Magalska, A., et al. Curcumin induces cell death without oligonucleosomal DNA fragmentation in quiescent and proliferating human CD8+ cells. Acta Biochimica Polonica. 53(3): 531-538, 2006.
- Maheshwari, R., et al. Multiple biological activities of curcumin: a short review. Life Sciences. 78(18): 2081-2087, 2006.
- Mathuria, N. and Verma, R. Ameliorative effect of curcumin on aflatoxin-induced toxicity in DNA, RNA and protein in liver and kidney of mice. Acta Poloniae Pharmaceutica. 64(6): 497-502, 2007.
- Monograph. Curcuma longa (turmeric). Alternative Medicine Review. 6(suppl): S62-S66, 2001.
- Morimitsu, Y., et al. A sulforaphane analogue that potently activates the Nrf2-dependent detoxification pathway. Journal of Biological Chemistry. 277(5): 3456-3463, 2002.
- Myzak, M. and Dashwood, R. Chemoprotection by sulforaphane: keep one eye beyond Keap1. Cancer Letters. 233(2): 208-218, 2006.
- Myzak, M., et al. Sulforaphane inhibits histone deacetylase in vivo and suppresses tumorigenesis in Apc-minus mice. FASEB. 20(3): 506-508, 2006.
- Naik, R., et al. Protection of liver cells from ethanol cytotoxicity by curcumin in liver slice culture in vitro. Journal of Ethnopharmacology. 95(1): 31-37, 2004.
- Nanji, A., et al. Curcumin prevents alcohol-induced liver disease in rats by inhibiting the expression of NF-kappa B-dependent genes. American Journal of Physiology. 284(2): G321-G327, 2003.
- Ng, T., et al. Curry consumption and cognitive function in the elderly. American Journal of Epidemiology. 164(9): 898-906, 2006.
- Nishinaka, T., et al. Curcumin activates human glutathione S-transferase P1 expression through antioxidant response element. Toxicology Letters. 170(3): 238-247, 2007.
- Noyan-Ashraf, M., et al. Dietary approach to decrease aging-related CNS inflammation. Nutritional Neuroscience. 8(2): 101-110, 2005.
- O’Connell, M. and Rushworth, S. Curcumin: potential for hepatic fibrosis therapy? British Journal of Pharmacology. 153(3): 403-405, 2007.
- Osawa, T. Nephroprotective and hepatoprotective effects of curcuminoids. Advances in Experimental Medicine and Biology. 595: 407-423, 2007.
- Pal, S., et al. Amelioration of immune cell number depletion and potentiation of depressed detoxification system of tumor-bearing mice by curcumin. Cancer Detection and Prevention. 29(5): 470-478, 2005.
- Pari, L. and Amali, D. Protective role of tetrahydrocurcumin (THC) an active principle of turmeric on chloroquine induced hepatotoxicity in rats. Journal of Pharmacy and Pharmaceutical Sciences. 8(1): 115-123, 2005.
- Perkins, S., et al. Chemopreventive efficacy and pharmacokinetics of curcumin in the min/+ mouse, a model of familial adenomatous polyposis. Cancer Epidemiology, Biomarkers, and Prevention. 11(6): 535-540, 2002.
- Rushworth, S., et al. Role of protein kinase C delta in curcumin-induced antioxidant response element-mediated gene expression in human monocytes. Biochemical and Biophysical Research Communications. 341(4): 1007-1016, 2006.
- Salvioli, S., et al. Curcumin in cell death processes: A challenge for CAM of age-related pathologies. Evidence-based Complementary and Alternative Medicine. 4(2): 181-190, 2007.
- Scapagnini, G., et al. Curcumin activates defensive genes and protects neurons against oxidative stress. Antioxidants and Redox Signaling. 8(3-4): 395-403, 2006.
- Shen, G., et al. Modulation of nuclear factor E2-related factor 2-mediated gene expression in mice liver and small intestine by cancer chemopreventive agent curcumin. Molecular and Cancer Therapeutics. 5(1): 39-51, 2006.
- Shen, S., et al. Protective effect of curcumin against liver warm ischemia/reperfusion injury in rat model is associated with regulation of heat shock protein and antioxidant enzymes. World Journal of Gastroenterology. 13(13): 1953-1961, 2007.
- Shishodia, S., et al. Curcumin: getting back to the roots. Annals of the New York Academy of Sciences. 1056: 206-217, 2005.
- Shu, J., et al. The study of therapeutic effects of curcumin on hepatic fibrosis and variation of correlated cytokine. Journal of Chinese Medicinal Materials. 30(11): 1421-1425, 2007.
- Shu, J., et al. Therapeutic effects of curcumin treatment on hepatic fibrosis. Chinese Journal of Hepatology. 15(10): 753-757, 2007.
- Shukla, P., et al. Protective effect of curcumin against lead neurotoxicity in rat. Human and Experimental Toxicology. 22(12): 653-658, 2003.
- Smith, T., et al. Allyl-isothiocyanate causes mitotic block, loss of cell adhesion and disrupted cytoskeletal structure in HT29 cells. Carcinogenesis. 25(8): 1409-1415, 2004.
- Srinivasan, M., et al. Protective effect of curcumin on gamma-radiation induced DNA damage and lipid peroxidation in cultured human lymphocytes. Mutation Research. 611(1-2): 96-103, 2006.
- Surh YJ. Anti-tumor promoting potential of selected spice ingredients with antioxidative and anti-inflammatory activities: a short review. Food Chem Toxicol 2002;40:1091-7.
- Tang, L., et al. Potent activation of mitochondria-mediated apoptosis and arrest in S and M phases of cancer cells by a broccoli sprout extract. Molecular Cancer Therapeutics. 5(4): 935-944, 2006.
- Thangapazham, R., et al. Multiple molecular targets in cancer chemoprevention by curcumin. AAPS Journal. 8(3): E443-E449, 2006.
- Thejass, P. and Kuttan, G. Antimetastatic activity of Sulforaphane. Life Sciences. 78(26): 3043-3050, 2006.
- Thejass, P. and Kuttan, G. Augmentation of natural killer cell and antibody-dependent cellular cytotoxicity in BALB/c mice by sulforaphane, a naturally occurring isothiocyanate from broccoli through enhanced production of cytokines IL-2 and IFN-gamma. Immunopharmacology and Immunotoxicology. 28(3): 443-457, 2006.
- Thejass, P. and Kuttan, G. Immunomodulatory activity of Sulforaphane, a naturally occurring isothiocyanate from broccoli (Brassica oleracea). Phytomedicine. 14(7-8): 538-545, 2007.
- Wakabayashi, N., et al. Protection against electrophile and oxidant stress by induction of the phase 2 response: fate of cysteines of the Keap1 sensor modified by inducers. Proceedings of the National Academy of Sciences of the United States of America. 101(7): 2040-2045, 2004.
- Wei, Q., et al. Inhibition of lipid peroxidation and protein oxidation in rat liver mitochondria by curcumin and its analogues. Biochimica et Biophysica Acta. 1760(1): 70-77, 2006.
- Wu, A., et al. Dietary curcumin counteracts the outcome of traumatic brain injury on oxidative stress, synaptic plasticity, and cognition. 197(2): 309-317, 2006.
- Xu, Y., et al. Curcumin reverses the effects of chronic stress on behavior, the HPA axis, BDNF expression and phosphorylation of CREB. Brain Research. 1122(1): 56-64, 2006.
- Yadav, V., et al. Immunomodulatory effects of curcumin. Immunopharmacology and Immunotoxicology. 27(3): 485-497, 2005.
- Yang, F., et al. Curcumin inhibits formation of amyloid beta oligomers and fibrils, binds plaques, and reduces amyloid in vivo. Journal of Biological Chemistry. 280(7): 5892-5901, 2005.
- Ye, S., et al. Effect of curcumin on the induction of glutathione S-transferases and NADP(H):quinone oxidoreductase and its possible mechanism of action. Acta Pharmaceutica Sinica. 42(4): 376-380, 2007.
- Zhang F, Altorki NK, Mestre JR, et al. Curcumin inhibits cyclooxygenase-2 transcription in bile acid- and phorbol ester-treated human gastrointestinal epithelial cells. Carcinogenesis 1999; 20:445-51.
- Zhang, L., et al. Curcuminoids enhance amyloid-beta uptake by macrophages of Alzheimer's disease patients. Journal of Alzheimer’s Disease. 10(1): 1-7, 2006.
- Zheng, S. and Chen, A. Curcumin suppresses the expression of extracellular matrix genes in activated hepatic stellate cells by inhibiting gene expression of connective tissue growth factor. American Journal of Physiology. 290(5): G883-G893, 2006.
- Zheng, S. and Chen, A. Disruption of transforming growth factor-beta signaling by curcumin induces gene expression of peroxisome proliferator-activated receptor-gamma in rat hepatic stellate cells. American Journal of Physiology. 292(1): G113-G123, 2007.
- Zheng, S., et al. De novo synthesis of glutathione is a prerequisite for curcumin to inhibit hepatic stellate cell (HSC) activation. Free Radical Biology and Medicine. 43(3): 444-453, 2007.
Heart Health™ Essential Omega III Fish Oil with Vitamin E:
- Astorga G, Cubillos A, Masson L, Silva JJ. Active rheumatoid arthritis: effect of dietary supplementation with omega-3 oils. A controlled double-blind trial. Rev Med Chil 1991;119:267-72.
- Bonaa, KH, et al, Effect of eicosapentaenoic and docosahexaenoic acids on blood pressure in hypertension. A population-based intervention trial from the Tromso study. N Engl J Med 322(12):795-801 (1990)
- Chan JK, et al, Dietary alpha-linolenic acid is as effective as oleic acid and linoleic acid in lowering blood cholesterol in normolipidemic men. Am J Clin Nutr 53(5):1230-1234 (1991)
- Fortin PR, Lew RA, Liang MH, et al. Validation of a meta-analysis: the effects of fish oil in rheumatoid arthritis. J Clin Epidemiol 1995;48:1379-90.
- Garrido A, et al, Ingestion of high doses of fish oil increases the susceptibility of cellular membranes to the induction of oxidative stress. Lipids 24(9):833-835 (1989)
- Goldberg RJ, Katz J. A meta-analysis of the analgesic effects of omega-3 polyunsaturated fatty acid supplementation for inflammatory joint pain. Pain 2007;129:210-23.
- Harris WS, et al, Dietary omega-3 fatty acids prevent carbohydrate-induced hypertriglyceridemia. Metabolism 33(11):1016-1019 (1984)
- Howe PR. Dietary fats and hypertension. Focus on fish oil. Ann NY Acad Sci 827:339-352 (1997)
- Kjeldsen-Kragh J, Lund JA, Riise T, et al. Dietary omega-3 fatty acid supplementation and naproxen treatment in patients with rheumatoid arthritis. J Rheumatol 1992;19:1531-6.
- Knapp HR, FitzGerald GA. The antihypertensive effects of fish oil. A controlled study of polyunsaturated fatty acid supplements in essential hypertension. J Engl J Med 320(16):1037-1043 (1989)
- Kris-Etherton PM, et al, fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease. Arterioscler Thromb Vasc Biol 23(2):e20-e30 (2003)
- Lau CS, Morley KD, Belch JJ. Effects of fish oil supplementation on non-steroidal anti-inflammatory drug requirement in patients with mild rheumatoid arthritis- a double-blind, placebo-controlled study. Br J Rheumatol 1993;32:982-9.
- Madsen T, Skou HA, et al, C-reactive protein, dietary n-3 fatty acids, and the extent of coronary artery disease. Am J Cardiol 88:1139-42 (2001)
- Morris MC, et al, The effect of fish oil on blood pressure in mild hypertensive subjects: a randomized crossover trial. Am J Clin Nutr 57(1):59-64 (1993)
- Morris, MC, Sacks F, Rosner B. Does fish oil lower blood pressure? A meta-analysis of controlled trials. Circulation 88(2):523-533 (19930
- Nestel PJ. Fish oil attenuates the cholesterol induced rise in lipoprotein cholesterol. Am J Clin Nutr 43(5):752-757 (1986)
- Rigelsky, JM, et al, Hawthorn: pharmacology and therapeutic uses. Am J Health Syst Pharm 59:417-22 (2002)
- Tsai PJ, Lu SC. Fish oil lowers plasma lipid concentrations and increases the susceptibility of low density lipoprotein to oxidative modification in healthy men. J Formos Med Assoc 96(9):718-726 (1997)
- van der Tempel H, Tulleken JE, Limburg PC, et al. Effects of fish oil supplementation in rheumatoid arthritis. Ann Rheum Dis 1990;49:76-80.
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