PROTANDIM Protandim is a one-a-day, all natural supplement that activates our body's internal defenses, our survival genes, to do what they were created to do – protect our cells from damage and disease.

Over time and around the age of 20, our genes, like the keys of a piano, get out of tune and no longer function at their peak performance: Aging and disease result from this - disharmony.

Protandim activates NRF-2, the master tuner within our cells, and brings our genes back to the perfect harmony and powerful function of our youth.

Independent research by Harvard, VCU, LSU and others, have validated this ability and measured Protandim's impact in tuning between 400 - 500 survival genes and what that means for our health and our battle against aging, cancer and heart disease. Additional studies are being conducted on osteoarthritis, diabetes, HIV/AIDS, periodontal disease, asthma, reduced injury recovery rates, and many others. Published peer-reviewed research demonstrates Protandim's ability to tune the following genes:

• Antioxidant - reducing oxidation/aging by over 40% • Glutathione — increasing by 300% • Anti-inflammatory • Anti-fibrotic genes — reducing scarring of the heart • P-53 - a tumor suppressor gene • Osteopontin - levels reduced by over 50%. — High levels of osteopontin accompany critical diseases by creating the environment for diseases to thrive and grow. • FABP-4 — associated with multiple pro-inflammatory responses - Protandim reduces by 85% • FABP -5 - reduces by 66% which lowers likelihood of calcified arteries • Akr 1 B10 - Promotes cell survival Protandim unleashes the power within, which is both safe and our powerful and proven first line of defense.

Summary of Peer-Reviewed Science on Protandim

Complete studies available at www.Pubmed.gov- search Protandim

1. Antioxidants for the Treatment of Patients with Severe Angioproliferative Pulmonary Hypertension. Voelkel NF, Bogaard HJ, Hussein AA, Farkas L, Gomez-Arroyo J, Nataraj an R.

Source: 1 Victoria Johnson Center for Lung Research, Virginia Commonwealth University , Richmond, Virginia.

Abstract: Abstract Significance: Pathobiological mechanisms that contribute to pulmonary vasoconstriction, lung vascular remodeling, and the development of right heart failure include the generation of reactive oxygen and nitrogen species and the response of lung vascular and cardiac cells to these molecules. We review the information regarding oxidant stress balanced by antioxidant mechanisms and the role of oxidants and antioxidants in hypoxic pulmonary hypertension and their potential role in an animal model of severe pulmonary arterial hypertension (PAH). Recent Advances: In human lung tissue from patients with idiopathic PAH, we find reduced superoxide dismutase activity and

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high expression of the oxidant stress markers nitrotyrosine and 8-OH-guanosine. In the Sugen 5416/chronic hypoxia model of PAH, lung tissue expression of nitrotyrosine and hemeoxygenase 1 (H0-1) is substantial, while HO-1 expression in the failing right ventricle is decreased. This model, based on administration of the VEGF receptor blocker Sugen 5416 and chronic hypoxia (Su/Hx), reproduces many of the characteristic features of severe angioobliterative human PAH. Treatment of Su/Hx rats with protandim, which nuclear factor erythroid-2 related factor (Nrf2)-dependently upregulates the expression of genes encoding antioxidant enzymes, protects against right heart failure without affecting angioobliterative PAH. Critical Issues: In human severe PAH, patient survival is determined by the function of the stressed right ventricle; investigation of oxidative and nitrosative stresses and their potential contribution to right heart failure is necessary. Future Directions: Antioxidant therapeutic strategies may be of benefit in the setting of human severe PAH. Whether antioxidant strategies affect lung vascular remodeling and/or prevent right heart failure remains to be examined. Antioxid. Redox Signal. 00, 000-000.

2. Phytochemical activation of Nrf2 protects human coronary artery endothelial cells against an oxidative challenge. Oxid Med Cell Longev. 2012;2012:132931. Epub 2012 May 22.Donovan EL, McCord JM, Reuland DJ, Miller BF, Hamilton KL. Source: Department of Health and Exercise Science, Colorado State University, 220 Moby B Complex 1582, Fort Collins, CO 80523, USA.

Abstract: Activation of NF-E2-related factor 2 (Nrf2) is a potential therapeutic intervention against endothelial cell oxidative stress and associated vascular disease. We hypothesized that treatment with the phytochemicals in the patented dietary supplement Protandim would induce Nrf2 nuclear localization and phase II antioxidant enzyme protein in human coronary artery endothelial cells (HCAECs), protecting against an oxidant challenge in an Nrf2- dependent manner. Protandim treatment induced Nrf2 nuclear localization, and HO-1 (778% of control ± 82.25 P < 0.01), SOD1 (125.9% of control ± 6.05 P < 0.01), NQO1 (126% of control ± 6.5 P < 0.01), and GR (119.5% of control ± 7.00 P < 0.05) protein expression in HCAEC. Treatment of HCAEC with H(2)0(2) induced apoptosis in 34% of cells while pretreatment with Protandim resulted in only 6% apoptotic cells (P < 0.01). Nrf2 silencing significantly decreased the Protandim-induced increase in HO-1 protein (P < 0.01). Nrf2 silencing also significantly decreased the protection afforded by Protandim against H(2)O(2)- induced apoptosis (P < 0.01 compared to no RNA, and P < 0.05 compared to control RNA). These results show that Protandim induces Nrf2 nuclear localization and antioxidant enzyme expression, and protection of HCAEC from an oxidative challenge is Nrf2 dependent.

3.Protandim does not influence alveolar epithelial permeability or intrapulmonary oxidative stress in human subjects with alcohol use disorders. Am J Physiol Lung Cell Mol Physiol. 2012 Apr 1;302(7):L688-99. doi: 10.1152/ajplung.00297.2011. Epub 2012 Jan 20.Burnham EL, McCord JM, Bose S, Brown LA, House R, Moss M, Gaydos J.

Source: Division of Pulmonary Sciences and Critical Care Medicine, Univ. of Colorado School of Medicine, Aurora, CO 80045, USA. Ellen.burnham@ucdenver.edu

Abstract: Alcohol use disorders (AUDs), including alcohol abuse and dependence, have been linked to the development of acute lung injury (ALI). Prior clinical investigations suggested an association between

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AUDs and abnormal alveolar epithelial permeability mediated through pulmonary oxidative stress that may partially explain this relationship. We sought to determine if correcting pulmonary oxidative stress in the setting of AUDs would normalize alveolar epithelial permeability in a double-blinded, randomized, placebo-controlled trial of Protandim, a nutraceutical reported to enhance antioxidant activity. We randomized 30 otherwise healthy AUD subjects to receive directly observed inpatient oral therapy with either Protandim (1,350 mg/day) or placebo. Subjects underwent bronchoalveolar lavage (BAL) and blood sampling before study drug administration and after 7 days of therapy; all AUD subjects completed the study protocol without adverse events. BAL total protein was measured at each timepoint as an indicator of alveolar epithelial permeability. In subjects with AUDs, before study drug initiation, BAL total protein values were not significantly higher than in 11 concurrently enrolled controls (P = 0.07). Over the 7-day study period, AUD subjects did not exhibit a significant change in BAL total protein, regardless of their randomization to Protandim = 14, -2% fintraquartile range (IQR), -56-146%)} or to placebo In = 16, 77% (IQR -20-290%); P = 0.19]. Additionally, among those with AUDs, no significant changes in BAL oxidative stress indexes, epithelial growth factor, fibroblast growth factor, interleukin-1P, or interleukin-10 were observed regardless of drug type received. Plasma thiobarbituric acid reactive substances, a marker of lipid peroxidation, decreased significantly over time among AUD subjects randomized to placebo (P < 0.01). These results suggest that Protandim for 7 days in individuals with AUDs who are newly abstinent does not alter alveolar epithelial permeability. However, our work demonstrates the feasibility of safely conducting clinical trials that include serial bronchoscopies in a vulnerable population at risk for acute lung injury.

4. Oxidative stress in health and disease: the therapeutic potential of Nrf2 activation. Mol Aspects Med. 2011 Aug;32(4-6):234-46. Epub 2011 Oct 15.Hybertson BM, Gao B, Bose SK, McCord JM.

Source:Department of Medicine, Division of Pulmonary Science and Critical Care Medicine, University of Colorado at Denver, Aurora, CO 80045, USA. brooks.hybertson@ucdenver.edu

Abstract: For the past 40 years or so, oxidative stress has been increasingly recognized as a contributing factor in aging and in various forms of pathophysiology generally associated with aging. Our view of oxidative stress has been largely "superoxide-centric", as we focused on the pathological sources of this oxygen-derived free radical and the types of molecular havoc it can wreak, as well as on the protection provided by the antioxidant enzymes, especially the superoxide dismutases, catalases, and glutathione peroxidases. In the last decade our view of oxidative stress has broadened considerably, and it is now often seen as an imbalance that has its origins in our genes, and the ways in which gene expression is regulated. At the center of this new focus is the transcription factor called nuclear factor (erythroid-derived 2)-like 2, or Nrf2. Nrf2 is referred to as the "master regulator" of the antioxidant response, modulating the expression of hundreds of genes, including not only the familiar antioxidant enzymes, but large numbers of genes that control seemingly disparate processes such as immune and inflammatory responses, tissue remodeling and fibrosis, carcinogenesis and metastasis, and even cognitive dysfunction and addictive behavior. Thus, the dysregulation of Nrf2-regulated genes provides a logical explanation for the connections, both direct and indirect, between observable oxidative stress and perhaps 200 human diseases involving these various physiological processes, each reflecting a network involving many gene products. The evolutionary self-association of these many genes under the common control of Nrf2 suggests that the immune and inflammatory systems may present the largest demand for increased

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antioxidant protection, apart from constitutive oxidative stress resulting from mitochondrial oxygen consumption for metabolic purposes. Gene expression microarray data on human primary vascular endothelial cells and on the SK-N-MC human neuroblastoma-derived cell line have been obtained in response to the dietary supplement Protandim, a potent composition of highly synergistic phytochemical Nrf2 activators. Pathway analysis of results shows significant modulation by Protandim of pathways involving not only antioxidant enzymes, but of those related to colon cancer, cardiovascular disease, and Alzheimer disease.

5. The role of manganese superoxide dismutase in skin cancer. Enzyme Res. 2011;2011:409295. Epub 2011 Mar 23. Robbins D, Zhao Y.

Source:Department of Pharmacology, Toxicology & Neuroscience, Louisiana State University Health Sciences Center, 1501 Kings Highway, Shreveport, LA 71130, USA.

Abstract: Recent studies have shown that antioxidant enzyme expression and activity are drastically reduced in most human skin diseases, leading to propagation of oxidative stress and continuous disease progression. However, antioxidants, an endogenous defense system against reactive oxygen species (ROS), can be induced by exogenous sources, resulting in protective effects against associated oxidative injury. Many studies have shown that the induction of antioxidants is an effective strategy to combat various disease states. In one approach, a SOD mimetic was applied topically to mouse skin in the two-stage skin carcinogenesis model. This method effectively reduced oxidative injury and proliferation without interfering with apoptosis. In another approach, Protandim, a combination of 5 well-studied medicinal plants, was given via dietary administration and significantly decreased tumor incidence and multiplicity by 33% and 57%, respectively. These studies suggest that alterations in antioxidant response may be a novel approach to chemoprevention. This paper focuses on how regulation of antioxidant expression and activity can be modulated in skin disease and the potential clinical implications of antioxidant-based therapies.

6. Protandim attenuates intimal hyperplasia in human saphenous veins cultured ex vivo via a catalase-dependent pathway. Free Radic Biol Med. 2011 Mar 15;50(6):700-9. Epub 2010 Dec 15. Joddar B, Reen RK, Firstenberg MS, Varadharaj S, McCord JM, Zweier JL, Gooch KJ.

Source:Department of Biomedical Engineering, The Ohio State University, Columbus, OH 43210, USA.

Abstract: Human saphenous veins (HSVs) are widely used for bypass grafts despite their relatively low long-term patency. To evaluate the role of reactive oxygen species (ROS) signaling in intima hyperplasia (IH), an early stage pathology of vein-graft disease, and to explore the potential therapeutic effects of up-regulating endogenous antioxidant enzymes, we studied segments of HSV cultured ex vivo in an established ex vivo model of HSV IH. Results showed that HSV cultured ex vivo exhibit an —3-fold increase in proliferation and —3.6-fold increase in intimal area relative to freshly isolated HSV. Treatment of HSV during culture with Protandim, a nutritional supplement known to activate Nrf2 and increase the expression of antioxidant enzymes in several in vitro and in vivo models, blocks IH and

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reduces cellular proliferation to that of freshly isolated HSV. Protandim treatment increased the activity of SOD, HO-1, and catalase 3-, 7-, and 12-fold, respectively, and decreased the levels of superoxide (0(2)(•-)) and the lipid peroxidation product 4-HNE. Blocking catalase activity by cotreating with 3- amino-1,2,4-triazole abrogated the protective effect of Protandim on III and proliferation. In conclusion, these results suggest that ROS-sensitive signaling mediates the observed IH in cultured HSV and that up-regulation of endogenous antioxidant enzymes can have a protective effect.

7. The Dietary Supplement Protandim Decreases Plasma Osteopontin and Improves Markers of Oxidative Stress in Muscular Dystrophy Mdx Mice. J Diet Suppl. 2010 Jun 1;7(2):159-178. Qureshi MM, McClure WC, Arevalo NL, Rabon RE, Mohr B, Bose SK, McCord JM, Tseng BS.

Source:Department of Pediatrics, Texas Tech University Health Sciences Center, Paul L. Foster School of Medicine, El Paso, TX. Earlier, he was associated with Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA.

Abstract:Therapeutic options for Duchenne muscular dystrophy (DMD), the most common and lethal neuromuscular disorder in children, remain elusive. Oxidative damage is implicated as a pertinent factor involved in its pathogenesis. Protandim((R)) is an over-the-counter supplement with the ability to induce antioxidant enzymes. In this study we investigated whether Protandim((R)) provided benefit using surrogate markers and functional measures in the dystrophin-deficient (mdx)mouse model of DMD. Male 3-week-old mdx mice were randomized into two treatment groups: control (receiving standard rodent chow) and Protandim((R))-supplemented standard rodent chow. The diets were continued for 6-week and 6-month studies. The endpoints included the oxidative stress marker thiobarbituric acid-reactive substances (TBARS), plasma osteopontin (OPN), plasma paraoxonase (PON1) activity, H&E histology, gadolinium-enhanced magnetic resonance imaging (MRI) of leg muscle and motor functional measurements. The Protandim((R)) chow diet in mdx mice for 6 months was safe and well tolerated. After 6 months of Protandim((R)), a 48% average decrease in plasma TBARS was seen; 0.92 nmol/mg protein in controls versus 0.48 nmoUmg protein in the Protandim((R)) group (p = .006). At 6 months, plasma OPN was decreased by 57% (p = .001) in the Protandim((R))-treated mice. Protandim((R)) increased the plasma antioxidant enzyme PON1 activity by 35% (p = .018). After 6 months, the mdx mice with Protandim((R)) showed 38% less MRI signal abnormality (p = .07) than mice on control diet. In this 6-month mdx mouse study, Protandim((R)) did not significantly alter motor function nor histological criteria.

8. The chemopreventive effects of Protandim: modulation of p53 mitochondrial translocation and apoptosis during skin carcinogenesis. PLoS One. 2010 Jul 30;5(7):e11902. Robbins D, Gu X, Shi R, Liu J, Wang F, Ponville J, McCord JM, Zhao Y.

Source:Department of Pharmacology, Toxicology and Neuroscience, Louisiana State University Health Sciences Center, Shreveport, Louisiana, United States of America.

Abstract: Protandim, a well defined dietary combination of 5 well-established medicinal plants, is known to induce endogenous antioxidant enzymes, such as manganese superoxide dismutase (MnSOD). Our previous studies have shown through the induction of various antioxidant enzymes, products of oxidative damage can be decreased. In addition, we have shown that tumor multiplicity and incidence can be

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decreased through the dietary administration of Protandim in the two-stage skin carcinogenesis mouse model. It has been demonstrated that cell proliferation is accommodated by cell death during DMBA/TPA treatment in the two-stage skin carcinogenesis model. Therefore, we investigated the effects of the Protandim diet on apoptosis; and proposed a novel mechanism of chemoprevention utilized by the Protandim dietary combination. Interestingly, Protandim suppressed DMBA/TPA induced cutaneous apoptosis. Recently, more attention has been focused on transcription-independent mechanisms of the tumor suppressor, p53, that mediate apoptosis. It is known that cytoplasmic p53 rapidly translocates to the mitochondria in response to pro-apoptotic stress. Our results showed that Protandim suppressed the mitochondrial translocation of p53 and mitochondrial outer membrane proteins such as Bax. We examined the levels of p53 and MnSOD expression/activity in murine skin JB6 promotion sensitive (P+) and promotion-resistant (P-) epidermal cells. Interestingly, p53 was induced only in P+ cells, not P- cells; whereas MnSOD is highly expressed in P- cells when compared to P+ cells. In addition, wild-type p53 was transfected into JB6 P- cells. We found that the introduction of wild-type p53 promoted transformation in JB6 P- cells. Our results suggest that suppression of p53 and induction of MnSOD may play an important role in the tumor suppressive activity of Protandim.

9. Chronic pulmonary artery pressure elevation is insufficient to explain right heart failure. Circulation. 2009 Nov 17;120(20):1951-60. Epub 2009 Nov 2.Bogaard HJ, Nataraj an R, Henderson SC, Long CS, Kraskauskas D, Smithson L, Ockaili R, McCord JM, Voelkel NF.

Source:Divisions of Pulmonary and Critical Care, Virginia Commonwealth University, Richmond, VA 23298-0281, USA. nvoelkel@mcvh-vcu.edu

Abstract

BACKGROUND:

The most important determinant of longevity in pulmonary arterial hypertension is right ventricular (RV) function, but in contrast to experimental work elucidating the pathobiology of left ventricular failure, there is a paucity of data on the cellular and molecular mechanisms of RV failure.

METHODS AND RESULTS:

A mechanical animal model of chronic progressive RV pressure overload (pulmonary artery banding, not associated with structural alterations of the lung circulation) was compared with an established model of angioproliferative pulmonary hypertension associated with fatal RV failure. Isolated RV pressure overload induced RV hypertrophy without failure, whereas in the context of angioproliferative pulmonary hypertension, RV failure developed that was associated with myocardial apoptosis, fibrosis, a decreased RV capillary density, and a decreased vascular endothelial growth factor mRNA and protein expression despite increased nuclear stabilization of hypoxia-induced factor-lalpha. Induction of myocardial nuclear factor E2-related factor 2 and heme-oxygenase 1 with a dietary supplement (Protandim) prevented fibrosis and capillary loss and preserved RV function despite continuing pressure overload.

CONCLUSIONS: These data brought into question the commonly held concept that RV failure associated with pulmonary hypertension is due strictly to the increased RV afterload.

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10. Protandim, a fundamentally new antioxidant approach in chemoprevention using mouse two-stage skin carcinogenesis as a model. PLoS One. 2009;4(4):e5284. Epub 2009 Apr 22. Liu J, Gu X, Robbins D, Li G, Shi R, McCord JM, Zhao Y.

Source:Department of Pharmacology, Toxicology & Neuroscience, Louisiana State University Health Sciences Center, Shreveport, Louisiana, United States of America.

Abstract: Oxidative stress is an important contributor to cancer development. Consistent with that, antioxidant enzymes have been demonstrated to suppress tumorigenesis when being elevated both in vitro and in vivo, making induction of these enzymes a more potent approach for cancer prevention. Protandim, a well-defined combination of widely studied medicinal plants, has been shown to induce superoxide dismutase (SOD) and catalase activities and reduce superoxide generation and lipid peroxidation in healthy human subjects. To investigate whether Protandim can suppress tumor formation by a dietary approach, a two-stage mouse skin carcinogenesis study was performed. At the end of the study, the mice on a Protandim-containing basal diet had similar body weight compared with those on the basal diet, which indicated no overt toxicity by Protandim. After three weeks on the diets, there was a significant increase in the expression levels of SOD and catalase, in addition to the increases in SOD activities. Importantly, at the end of the carcinogenesis study, both skin tumor incidence and multiplicity were reduced in the mice on the Protandim diet by 33% and 57% respectively, compared with those on basal diet. Biochemical and histological studies revealed that the Protandim diet suppressed tumor promoter-induced oxidative stress (evidenced by reduction of protein carbonyl levels), cell proliferation (evidenced by reduction of skin hyperplasia and suppression of PKC/JNK/Jun pathway), and inflammation (evidenced by reduction of ICAM-1IVCAM-1 expression, NF-kappaB binding activity, and nuclear p65/p50 levels). Overall, induction of antioxidant enzymes by Protandim may serve as a practical and potent approach for cancer prevention.

11. Synergistic induction of heme oxygenase-1 by the components of the antioxidant supplement Protandim. Free Radic Biol Med. 2009 Feb 1;46(3):430-40. Epub 2008 Nov 17. Velmurugan K, Alam J, McCord JM, Pugazhenthi S.

Source:Division of Endocrinology, Department of Medicine, University of Colorado Denver, Aurora, CO 80045, USA.

Abstract: Protandim is an antioxidant supplement that consists of five ingredients, namely, ashwagandha, bacopa extract, green tea extract, silymarin, and curcumin, each with known therapeutic properties. Protandim was formulated with the objective of combining multiple phytochemicals at low nontoxic doses to gain synergy among them. A recent clinical study demonstrated the in vivo antioxidant effects of Protandim (S.K. Nelson et al., 2006, Free Radic. Biol. Med. 40, 341-347). The objective of the present study was to determine if the components of Protandim induce heme oxygenase-1 (H0-1) in a synergistic manner in cultured MINE cells, a mouse beta-cell line, and in SK-N-MC cells, a human neuroblastoma cell line. When the components of Protandim were tested alone at low doses, curcumin showed minimal induction, whereas the others were unable to induce the HO-1 promoter, assayed by

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transient transfection. All components together, however, produced a strongly synergistic induction of around three- to ninefold in a dose-dependent manner, greatly exceeding the sum of the parts. Similar findings were obtained for the expression of HO-1 at the mRNA and protein levels. Protandim-mediated HO-1 induction involved the presence of ARE sites in the HO-1 promoter and nuclear translocalization of the transcription factor Nrf2, which binds to ARE sites. The involvement of multiple signaling pathways, including PI3-kinase/Akt, p38MAPK, and PKCdelta, in HO-1 induction seems to be the probable mechanism of synergy between the components of Protandim. There were significant increases in the levels of total glutathione in Protandim-treated cells. These findings suggest that the use of a combination of phytochemicals may be an efficient method for the induction of antioxidant enzymes.

12. The induction of human superoxide dismutase and catalase in vivo: a fundamentally new approach to antioxidant therapy. Free Radic Biol Med. 2006 Jan 15;40(2):341-7. Nelson SK, Bose SK, Grunwald GK, Myhill P, McCord JM.

Source:Webb-Waring Institute for Cancer, Aging and Antioxidant Research, University of Colorado Denver Health Sciences Center, Denver, CO 80262, USA.

Abstract: A composition consisting of extracts of five widely studied medicinal plants (Protandim) was administered to healthy human subjects ranging in age from 20 to 78 years. Individual ingredients were selected on the basis of published findings of induction of superoxide dismutase (SOD) and/or catalase in rodents in vivo, combined with evidence of decreasing lipid peroxidation. Each ingredient was present at a dosage sufficiently low to avoid any accompanying unwanted pharmacological effects. Blood was analyzed before supplementation and after 30 and 120 days of supplementation (675 mg/day). Erythrocytes were assayed for SOD and catalase, and plasma was assayed for lipid peroxidation products as thiobarbituric acid-reacting substances (TBARS), as well as uric acid, C-reactive protein, and cholesterol (total, LDL, and HDL). Before supplementation, TBARS showed a strong age-dependent increase. After 30 days of supplementation, TBARS declined by an average of 40% (p = 0.0001) and the age-dependent increase was eliminated. By 120 days, erythrocyte SOD increased by 30% (p < 0.01) and catalase by 54% (p < 0.002). We conclude that modest induction of the catalytic antioxidants SOD and catalase may be a much more effective approach than supplementation with antioxidants (such as vitamins C and E) that can, at best, stoichiometrically scavenge a very small fraction of total oxidant production.

Oxidative Stress! Linked to: ALL Cancer, Heart Disease, HIV/AIDS, Asthma,

Alzheimer's, Renal Failure, Depression, Periodontal disease, MS, over 105,000 studies on pubmed.gov!

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Protandim's Natural Ingredients

Milk Thistle Extract Used for thousands of years to improve health.

acopa Extract A serious free -radical scavenger.

Ashwagandha Supports a healthy immune system.

ET urmeric Extract Powerful contributor to Protandim's Nrf2 activation.

Green Tea Extract Contains important antioxidants.

Protandim is a supplement that combats oxidative stress through Nrf2 activation. Oxidative stress happens in everyone. Protandim significantly reduces oxidative stress through Nrf2 activation. Nrf2 regulates survival genes.

):\ idati stre ss , generated through the process of living life (eating, sleeping, breathing, exercising), is inevitable for everyone, but LifeVantage has the solution: Protandim, the Nrf2 Synergizer, the most important dietary supplement of our time.

Comprised of natural plant ingredients, Protandim is a patented, science -based, research-backed formula that has been tested and validated by renowned universities and institutions. It is the only supplement clinically proven to reduce oxidative stress in humans by an average of 40 percent in 30 days.

Protandim activates Nrf2, which communicates with cells, instructing them to do what they're already designed to do: up-regulate "survival genes," genes that enable cells to survive in the face of stress from free radicals and other oxidants, and down-regulates other genes that promote inflammation and fibrosis to help the body function at an optimal level.

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Not able to tell the difference between a 80 year old man's blood under a microscope to a 20 year olds in 30 days one tablet daily ...less than a cup of coffee a day to roll back the stress of time in your blood.

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*Nrf2 fights oxidative stress. *Nrf2 helps the body regulate at peak efficiency.

Nrf2, a protein messenger that binds itself to DNA, is the master regulator of the body's aging process and is critical in the fight against oxidative stress.

Nrf2 communicates with cells, instructing them to do what they're already designed to do. When activated, Nrf2 enters the nucleus of a cell and up-regulates "survival genes," genes that enable cells to survive in the face of stress from free radicals and other oxidants, and down-regulates other genes that promote inflammation and fibrosis to help the body function at an optimal level.

Protandim Activates the Antioxidant Defense

Superoxide dismutase, better known as SOD, is an important antioxidant defense in nearly all cells exposed to oxygen. LifeVantage Chief Science Officer Dr. Joe McCord discovered this enzyme in 1969. SOD is turned on by Nrf2 and is made by most cells to detoxify superoxide, a compound that the immune system deploys to destroy invading microorganisms.

More information go to: www.youngerblood.info To Order go to: www.YoungerBlood.com

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*Nrf2 fights oxidative stress. *Nrf2 helps the body regulate at peak efficiency.

Nrf2, a protein messenger that binds itself to DNA, is the master regulator of the body's aging process and is critical in the fight against oxidative stress.

Nrf2 communicates with cells, instructing them to do what they're already designed to do. When activated, Nrf2 enters the nucleus of a cell and up-regulates "survival genes," genes that enable cells to survive in the face of stress from free radicals and other oxidants, and down-regulates other genes that promote inflammation and fibrosis to help the body function at an optimal level.

Protandim Activates the Antioxidant Defense

Superoxide dismutase, better known as SOD, is an important antioxidant defense in nearly all cells exposed to oxygen. LifeVantage Chief Science Officer Dr. Joe McCord discovered this enzyme in 1969. SOD is turned on by Nrf2 and is made by most cells to detoxify superoxide, a compound that the immune system deploys to destroy invading microorganisms.