MEDICAL PROFESSIONALS

 

STUDY 1

Dr. Joe McCord Explains the Significance of the Ohio State University Study - Heart Health.

Protandim Attenuates Intimal Hyperplasia in Human SaphenousVeins Cultured  Ex Vivo via a Catalase-Dependent Pathway

OHIO STATE UNIVERSITY

Free Radical Biology and Medicine (2010)

Abstract: 

Human saphenous veins (HSV) are widely used for bypass graphs despite their relatively low long-term patency. 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 in segments of HSV cultured ex vivo in an established ex vivo model of HSV IH. Protandim®, known to activate Nrf2 and increase the expression of endogenous antioxidant enzymes in several in vitro and in vivo models, was used in this study.

Findings: 

Protandim® inhibits the formation of IH and the increase in cellular proliferation in HSV cultured ex-vivo. Further, Protandim® attenuates rise in superoxide (O) levels in HSV, attenuates rise in lipid peroxidation (4-HNE) levels in HSV, enhances increases in the activities of HO-1, total SOD and catalase in HSV, enhances the protein level and immunofluorescent intensity of catalase in HSV, blocks medial thickening as well as cellular proliferation in established ex-vivo model of the early stages of vein-graft disease. These abilities of Protandim®, as demonstrated in HSV harvested from patients undergoing coronary artery bypass grafting, makes it an attractive candidate for future consideration as a pharmacological treatment of vein-graft failure.

 

STUDY 2

Nrf2, a master regulator of detoxification and also antioxidant, anti-inflammatory and other cytoprotective mechanisms, is raised by health promoting factors.

Washington STATE UNIVERSITY

NRF2 Research (2015)

Abstract:

The transcription factor Nrf2, nuclear factor erythroid-2-related factor 2, activates the transcription of over 500 genes in the human genome, most of which have cytoprotective functions. Nrf2 produces cytoprotection by detoxification mechanisms leading to increased detoxification and excretion of both organic xenobiotics and toxic metals; its action via over two dozen genes increases highly coordinated antioxidant activities; it produces major anti-inflammatory changes; it stimulates mitochondrial biogenesis and otherwise improves mitochondrial function; and it stimulates autophagy, removing toxic protein aggregates and dysfunctional organelles. Health-promoting nutrients and other factors act, at least in part by raising Nrf2 including: many phenolic antioxidants; gamma- and delta-tocopherols and tocotrienols; long chain omega-3 fatty acids DHA and EPA; many carotenoids of which lycopene may be the most active; isothiocyanates from cruciferous vegetables; sulfur compounds from allium vegetables; terpenoids. Other health promoting, Nrf2 raising factors include low level oxidative stress (hormesis), exercise and caloric restriction. Raising Nrf2 has been found to prevent and/or treat a large number of chronic inflammatory diseases in animal models and/or humans including various cardiovascular diseases, kidney diseases, lung diseases, diseases of toxic liver damage, cancer (prevention), diabetes/metabolic syndrome/obesity, sepsis, autoimmune diseases, inflammatory bowel disease, HIV/AIDS and epilepsy. Lesser evidence suggests that raising Nrf2 may lower 16 other diseases. Many of these diseases are probable NO/ONOO(-) cycle diseases and Nrf2 lowers effects of NO/ONOO(-) cycle elements. The most healthful diets known, traditional Mediterranean and Okinawan, are rich in Nrf2 raising nutrients as apparently was the Paleolithic diet that our ancestors ate. Modern diets are deficient in such nutrients. Nrf2 is argued to be both lifespan and healthspan extending. Possible downsides to too much Nrf2 are also discussed. Nrf2 is not a magic bullet but is likely to be of great importance in health promotion, particularly in those regularly exposed to toxic chemicals.

Key Note:

While no doubt it is too early to make a conclusion, it is difficult to escape the suggestion, from Tables 1 and 4, that we may be on the verge of a new literature on health effects of 

Nrf2 which may well become the most extraordinary therapeutic and most extraordinary preventive breakthrough in the history of medicine.

 It is our opinion that raising Nrf2 is likely to be the most important health promoting approach into the foreseeable future. (p.11)

 

STUDY 3

Dr. Joe McCord explains the significance of the Baylor University Study - Chemosensitization Curcumin, the golden spice from Indian saffron, is a chemosensitizer and radiosensitizer for tumors and chemoprotector and radioprotector for normal organs.

BAYLOR UNIVERSITY MEDICAL CENTER DALLAS TEXAS

Nutrition and cancer. (2010)

Abstract: 

Chemosensitization has been observed in cancers of the breast, colon, pancreas, gastric, liver, blood, lung, prostate, bladder, cervix, ovary, head and neck, and brain and in multiple myeloma, leukemia, and lymphoma. Similar studies have also revealed that this agent can sensitize a variety of tumors to gamma radiation including glioma, neuroblastoma, cervical carcinoma, epidermal carcinoma, prostate cancer, and colon cancer. How curcumin acts as a chemosensitizer and radiosensitizer has also been studied extensively. For example, it downregulates various growth regulatory pathways and specific genetic targets including genes for NF-κB, STAT3, COX2, Akt, antiapoptotic proteins, growth factor receptors, and multidrug-resistance proteins. Although it acts as a chemosensitizer and radiosensitizer for tumors in some cases, curcumin has also been shown to protect normal organs such as liver, kidney, oral mucosa, and heart from chemotherapy and radiotherapy-induced toxicity.

Summary: 

The protective effects of curcumin appear to be mediated through its ability to induce the activation of NRF2 and induce the expression of antioxidant enzymes These preclinical studies are expected to lead to clinical trials to prove the potential of this age-old golden spice for treating cancer patients.

 

STUDY 4

The Induction of Human Superoxide Dismutase and Catalase In Vivo: A Fundamentally New Approach to Antioxidant Therapy.

UNIVERSITY OF COLORADO DENVER

 

Free Radical Biology and Medicine (2006)

Abstract: 

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.

Summary: 

Protandim® completely eliminates the usual age related increase in cell aging markers by decreasing the indicators of oxidative stress (TBARS) by 40% in 30 days, and by increasing cellular production of antioxidant enzymes superoxide dismutase (SOD) by 30% and catalase (CAT) by 54% by 120 days.

 

STUDY 5

Synergistic Induction of Heme Oxygenase-1 by the Components of an Antioxidant Supplement Protandim® (glutathione +300%).

UNIVERSITY OF COLORADO DENVER

Free Radical Biology and Medicine (2009)

Abstract: 

Protandim® is a supplement formulated with the objective of combining multiple phytochemicals at low non-toxic doses to gain synergy for induction of endogenous antioxidant enzymes. All components together produced a strongly synergistic induction of around three to ninefold, greatly exceeding the sum of the parts, and strongly suggesting this may be an effective method for the induction of antioxidant enzymes.

Conclusion: 

Protandim® produces a 300% increase in the cellular production of glutathione. As a key antioxidant, glutathione plays critical roles in the regenesis of other antioxidants (vitamins C and E), liver detoxification and elimination, and tissue repair. Further, Protandim® was shown to be a Nrf2 Activator. Findings show nuclear translocation of Nrf2 to the Antioxidant Response Element sites of genes on the DNA. Nrf2 then “re-tunes” the associated genes to function optimally.

 

STUDY 6

Protandim, a Fundamentally New Antioxidant Approach in Chemoprevention Using Mouse Two-Stage Skin Carcinogenesis as a Model.

LOUISIANA STATE UNIVERSITY

PLoS One Journal (2009)

Abstract: 

Biochemical and histological studies revealed that the Protandim diet suppressed tumor promoter – induced oxidative stress, cell proliferation, and inflammation. “Overall, induction of antioxidant enzymes by Protandim® may serve as a practical and potent approach for cancer prevention.”

Conclusions: 

Protandim® supplemented mice showed a 33% reduction in skin tumor incidence and a 57% reduction in tumor multiplicity. The mice receiving the diet without Protandim® supplementation developed cancer tumors 100% of the time.

 

STUDY 7

Chronic Pulmonary Artery Pressure Elevation is Insufficient to Explain Right Heart Failure

VIRGINIA COMMONWEALTH UNIVERSITY

American Heart Association Journal, Circulation (2009)

Abstract: 

Clinical Perspective - Protandim® can prevent Right Ventricular (RV) dysfunction and pathological remodeling in the setting of persistent pressure overload. “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: 

“Protandim® also prevented the death of heart cells and significantly lowered osteopontin (OPN-1) levels by more than 50%.” Protandim® has the ability “to effectively activate the transcription factor Nrf2, a signal to the cell’s DNA to increase expression of a network of antioxidants, anti-inflammatory, and anti-fibrotic genes.” Nrf2 preserves the expression of vascular endothelial growth factor and prevents RV failure without modifying lung angioproliferation.

 

STUDY 8

The Dietary Supplement Protandim® Decreases Plasma Osteopontin and Improves Markers of Oxidative Stress in Muscular Dystrophy Mdx Mice.

HARVARD UNIVERSITY

Informa Healthcare (2010)

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 nmol/mg 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.

Conclusions: 

“Oxidative stress is a significant pathologic factor in DMD.” After 6 months of Protandim® supplementation, a 48% decrease in plasma TBARS was seen, plasma OPN [osteopontin] was decreased by 57%, plasma antioxidant enzyme PON 1 activity was increased by 35%, and 38% less signal abnormality was shown.

 

STUDY 9

The Chemo-preventive Effects of Protandim: Modulation of p53 Mitochondrial Translocation and Apoptosis during Skin Carcinogenesis.

LOUISIANA STATE UNIVERSITY

PLoS ONE Journal (2010)

Abstract: 

Our results that suppression of p53 and induction of MnSOD may play an important role in the tumor suppressive activity of Protandim.

Results: 

MnSOD, highly inducible by Protandim, is effective in the suppression of tumor promotion. Previous findings were confirmed and extended that “Protandim® modulates tumorigenesis via the induction of endogenous antioxidant enzymes.” Additionally, “Protandim utilizes multiple mechanisms to modulate cell proliferation and aptosis in vivo and in vitro, which both contribute to tumorigenesis, therapies in chemoprevention.”

 

STUDY 10

Protandim Attenuates Intimal Hyperplasia in Human Saphenous Veins Cultured Ex Vivo via a Catalase-Dependent Pathway

OHIO STATE UNIVERSITY

 

Free Radical Biology and Medicine (2010)

Abstract: 

Human saphenous veins (HSV) are widely used for bypass graphs despite their relatively low long-term patency. 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 in segments of HSV cultured ex vivo in an established ex vivo model of HSV IH. Protandim®, known to activate Nrf2 and increase the expression of endogenous antioxidant enzymes in several in vitro and in vivo models, was used in this study.

Results: 

Protandim® inhibits the formation of IH and the increase in cellular proliferation in HSV cultured ex-vivo. Further, Protandim® attenuates rise in superoxide (O) levels in HSV, attenuates rise in lipid peroxidation (4-HNE) levels in HSV, enhances increases in the activities of HO-1, total SOD and catalase in HSV, enhances the protein level and immunofluorescent intensity of catalase in HSV, blocks medial thickening as well as cellular proliferation in established ex-vivo model of the early stages of vein-graft disease. These abilities of Protandim®, as demonstrated in HSV harvested from patients undergoing coronary artery bypass grafting, makes it an attractive candidate for future consideration as a pharmacological treatment of vein-graft failure.

 

STUDY 11

The Role of Manganese Superoxide Dismutase in Skin Cancer

LOUISIANA STATE UNIVERSITY

Enzyme Research (2011)

“The induction of antioxidant enzymes via dietary administration of Protandim® modulates both TPA-mediated cell proliferation and p53-mediated apoptotic signaling. Therefore, it can be concluded that oxidative stress forms a mechanistic linkage between cell proliferation, inflammation, and apoptosis, suggesting that potent multimodal antioxidant inducers may potentially be utilized with conventional chemotherapeutics.”

Universities and Institutions around the world continue to initiate and fund their own trials investigating its anti-aging and health-promoting capabilities. These include:

Massachusetts General Hospital, Harvard Medical School

Children’s Hospital, Denver

University of Florida

University of Kentucky

University of Michigan

University of Minnesota

Vanderbilt University

Glamorgan University, Wales

Sahigrenska University Hospital, Goteborg, Sweden

University of Toronto/St. Michelle’s Hospital, Canada

University Hospital, Brno, Czech Republic

Mexican Institute of Social Security, Mexico City

National Institute of Arthritis and Musculo Skeletal and Skin Diseases

 

MORE STUDIES

 

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Before you consider taking another competing product, we strongly advise that you visit and search https://www.ncbi.nlm.nih.gov/pubmed/ to see if the competing product has any Peer-Reviewed studies published.

Any company with substantial claims should submit a Peer-Reviewed study so the community can trust that the claims made are valid.