Although there are no studies of the product itself, many studies of the various active ingredients in the product are available.

 

 These are some the published research studies available (Click on , the summary of the article will appear):

Habitual dietary intake of β-carotene, vitamin C, folate, or vitamin E may interact with single nucleotide polymorphism on brachial-ankle pulse wave velocity in healthy adults.

European Journal of Nutrition – April 2015 [http://www.ncbi.nlm.nih.gov/pubmed/25869180]

CONCLUSION:   Greater dietary intake of these nutrients may protect those that are genetically vulnerable to stiffening of the arteries.

The association between vitamin E intake and hypertension: results from re-analysis of the National Health and Nutrition Survey.

Journal of Nutritional Science and Vitaminology (Tokyo) – 2014 [http://www.ncbi.nlm.nih.gov/pubmed/25297612]

CONCLUSION:   In summary, re-analysis of data from NHNS has revealed that higher vitamin E intake was significantly associated with lower prevalence of hypertension.

Estimation of plasma vitamin A, C and E levels in patients with metabolic syndrome.

Polski merkuriusz lekarski – May 2014 [http://www.ncbi.nlm.nih.gov/pubmed/24964509]

CONCLUSION:   The decreased level of vitamins A, C and E points to the weakening of the antioxidative barrier in patients with metabolic syndrome.

Antioxidant effects of vitamins C and E on the low-density lipoprotein oxidation mediated by myeloperoidase(MPO).

Iranian Biomedical Journal – 2013 [http://www.ncbi.nlm.nih.gov/pubmed/23279831]

CONCLUSION:   It can be concluded from results that vitamin C is able to improve LDL resistance to oxidative modification in vitro. In addition, vitamin C might be effective in LDL oxidation mediated by MPO in vivo, resulting in reduction of atherosclerosis process rate.

Does vitamin C or its combination with vitamin E improve radial artery endothelium-dependent vasodilatation in patients awaiting coronary bypass surgery?

Cardiovascular Journal of Africa – August 2013 [http://www.ncbi.nlm.nih.gov/pubmed/24217301]

CONCLUSION:   Vitamin C or its combination with vitamin E significantly enhanced endothelium-dependent vasodilatation in the radial circulation of patients with coronary artery disease.

Anti-atherosclerotic effects of a mixture of ascorbic acid, lysine, proline, arginine, cysteine, and green tea phenolics in human aortic smooth muscle cells.

Journal of Cardiovascular Pharmacology – March 2007 [http://www.ncbi.nlm.nih.gov/pubmed/17414225]

CONCLUSION:   The data suggest that this nutrient mixture has potential in blocking the development of atherosclerotic lesions by inhibiting atherogenic responses of vascular smooth muscle cells to pathologic stimuli and warrants in vivo studies.

Antioxidant vitamins and coronary heart disease risk: a pooled analysis of 9 cohorts.

American Journal of Clinical Nutrition – Dec 2004 [http://www.ncbi.nlm.nih.gov/pubmed/15585762]

CONCLUSION:   The results suggest a reduced incidence of major coronary heart disease events at high supplemental vitamin C intakes. The risk reductions at high vitamin E or vitamin A intakes appear to be small.

Vitamin C and vitamin E antagonistically modulate human vascular endothelial and smooth muscle cell DNA synthesis and proliferation.

European journal of nutrition – February 2002 [http://www.ncbi.nlm.nih.gov/pubmed/11990005]

CONCLUSION:   Vitamin C and E, alone or in combination, modulate proliferation and DNA synthesis of human arterial endothelial and muscle cells and this modulation is antagonistic. Thus, vitamin C and E may act “preventive” on atherosclerotic plaque formation in two steps: first re-endothelialisation is promoted, then human arterial smooth muscle cell growth is inhibited.

Nutritional strategies in cardiovascular disease control: an update on vitamins and conditionally essential nutrients.

Progress in cardiovascular nursing – 1999 [http://www.ncbi.nlm.nih.gov/pubmed/10689723]

ABSTRACT:   Several nutritional interventions for cardiovascular disease (CVD) prevention and therapy have recently appeared in the biomedical literature. These include appropriate use of several vitamins (E, C, B6, folate) and conditionally essential nutrients (CoQ10, L-arginine, propionyl L-carnitine). Possible undesirable consequences of long term nutritional supplementation with vitamin E and of adverse drug-nutrient interactions between the statins and CoQ10 are also considered. Although additional intervention studies are needed, current scientific evidence generally supports nutritional supplementation with these nutrients as an effective adjunctive strategy for CVD control.

A review of vitamins A, C, and E and their relationship to cardiovascular disease.

Clinical excellence for nurse practitioners – 1998 [http://www.ncbi.nlm.nih.gov/pubmed/12675072]

CONCLUSION:   Targeted antioxidant vitamin intake should be included in CVD risk assessment and primary preventive counselling efforts.

Food intake, dietary supplements and survival time of scorbutic guinea pigs.

Nutrition & Metabolism – 1976 [http://www.ncbi.nlm.nih.gov/pubmed/958649]

CONCLUSION:   These findings could indicate that ascorbic acid has essential biochemical functions in addition to its involvement in the hydroxylation of proline and lysine.

Impact of administration of folic acid on selected indicators of inflammation in patients with primary arterial hypertension.

Postȩpy higieny i medycyny doświadczalnej (Online) – April 2015 [http://www.ncbi.nlm.nih.gov/pubmed/25897102]

CONCLUSION:   Administration of folic acid to persons with primary arterial hypertension in a dose of 15 mg/ day for 45 days caused a decrease in the concentration of homocysteine in serum. That could indirectly result in the decrease in concentrations of the indicators of inflammation (hsCRP, ICAM-1 and VCAM-1), as it is apparent from previous studies that hyperhomocysteinemia stimulates the synthesis of CRP and the expression of adhesion molecules.

Efficacy of folic acid supplementation in stroke prevention: a meta-analysis.

Lancet – June 2007 [http://www.ncbi.nlm.nih.gov/pubmed/17544768]

CONCLUSION:   Our findings indicate that folic acid supplementation can effectively reduce the risk of stroke in primary prevention.

Folic acid says NO to vascular diseases.

Nutrition – July – August 2003 [http://www.ncbi.nlm.nih.gov/pubmed/12831960]

CONCLUSION:   The common mechanism by which folic acid, H(4)B, vitamin C, omega-3 fatty acids, and L-arginine bring about their beneficial actions in various vascular diseases is by enhancing endothelial Nitric Oxide production. Hence, it remains to be determined whether a judicious combination of folic acid, vitamins B12, B6, and C, H(4)B, L-arginine, and omega-3 fatty acids in appropriate amounts may form a novel approach in the prevention and management of various conditions such as hyperlipidaemias, coronary heart disease, atherosclerosis, peripheral vascular disease, and some neurodegenerative conditions.

Investigating the cardio-protective abilities of supplemental L-arginine on parameters of endothelial function in a hypercholesterolemic animal model.

Journal of nutritional science and vitaminology – 2014 [http://www.ncbi.nlm.nih.gov/pubmed/25078369]

CONCLUSION:   Based on the results of this study, L-arginine appears to be a novel cardio-protective agent, illustrated by its ability to ameliorate the deleterious effects of hypercholesterolemia on endothelial function, in a manner comparable to, and sometimes more potent than, commonly used cardiovascular medications.

L-arginine attenuates oxidative stress condition during cardiomyopathy.

Indian journal of biochemistry & biophysics – April 2013 [http://www.ncbi.nlm.nih.gov/pubmed/23720883]

CONCLUSION:   Thus, it is inferred that L-arginine attenuates the oxidative stress conditions along with maintaining the blood pressure rate of patients suffering from cardiomyopathy.

Arginine bioavailability ratios are associated with cardiovascular mortality in patients referred to coronary angiography.

Atherosclerosis – September 2011[http://www.ncbi.nlm.nih.gov/pubmed/21632053]

CONCLUSION:   Global arginine bioavailability and the arginine to ornithine ratio are associated with markers of endothelial dysfunction and increased risk of cardiovascular mortality. Further studies are warranted to elucidate the pathobiology and clinical relevance of the arginine bioavailability ratios in cardio-metabolic diseases.

Therapeutic role of L-arginine on free radical scavenging system in ischemic heart diseases.

Indian journal of biochemistry & biophysics – December 2009 [http://www.ncbi.nlm.nih.gov/pubmed/20361713]

CONCLUSION:   The present study demonstrates that L-arginine administration may be beneficial to patients with myocardial ischemic disorders, such as acute myocardial infarction and acute angina.

Oral administration of L-arginine in patients with angina or following myocardial infarction may be protective by increasing plasma superoxide dismutase and total thiols with reduction in serum cholesterol and xanthine oxidase.

Oxidative medicine and cellular longevity – September October 2009 [http://www.ncbi.nlm.nih.gov/pubmed/20716909]

CONCLUSION:  These findings suggest that the supplementation of L-arginine along with regular therapy may be beneficial to the patients of ischemic myocardial syndromes.

L-arginine improves endothelial function and reduces LDL oxidation in patients with stable coronary artery disease

Clinical nutrition – December 2005 [http://www.ncbi.nlm.nih.gov/pubmed/16140428]

CONCLUSION:   Oral L-arginine supplement improved endothelial function and reduced LDL oxidation in stable CAD patients.

Effects of vitamin C on intracoronary L-arginine dependent coronary vasodilatation in patients with stable angina.

Heart – October 2005 [http://www.ncbi.nlm.nih.gov/pubmed/16162626]

CONCLUSION:   L-arginine dependent coronary segment vasodilatation was augmented by the antioxidant vitamin C in patients with coronary artery disease. Thus, vitamin C may have beneficial effects on nitric oxide bioavailability induced by L-arginine.

Lack of antioxidant activity of the antiatherogenic compound L-arginine.

Atherosclerosis – October 1999 [http://www.ncbi.nlm.nih.gov/pubmed/10532688]

CONCLUSION:  L-Arginine has only weak and non-specific antioxidant effects, suggesting that its major cardio-protective benefits occur through other mechanisms, such as via the nitric oxide pathway.

Hypoascorbemia induces atherosclerosis and vascular deposition of lipoprotein(a) in transgenic mice.

American Journal of Cardiovascular Disease – March 2015 [http://www.ncbi.nlm.nih.gov/pubmed/26064792]

CONCLUSION:   The result suggests that dietary ascorbate deficiency is a risk factor for atherosclerosis independent of dietary lipids. We provide support for the concept that Lp(a) functions as a mobile repair molecule compensating for the structural impairment of the vascular wall, a morphological hallmark of hypoascorbemia and scurvy

Plasma vitamin C and risk of hospitalisation with diagnosis of arterial fibrillation in men and woman in EPIC-Norfolk prospective study.

International Journal of Cardiology – December 2014 [http://www.ncbi.nlm.nih.gov/pubmed/25465828]

CONCLUSION:   Our findings suggest that intake of vitamin C might be preventative of arterial fibrillation with significant benefit particularly in women with baseline intake.

Combined metoprolol and ascorbic acid treatment prevents intrinsic damage to the heart during diabetic cardiomyopathy.

Canadian Journal of Physiological Pharmacology – October 2014 [http://www.ncbi.nlm.nih.gov/pubmed/25229873]

CONCLUSION:   While both drugs improved function, only ascorbic acid had effects on oxidative damage. Combination treatment strategy had a more pronounced improvement in function. Our β-blocker + antioxidant strategy focused on oxidative stress, not diabetes; therefore, it may prove useful in other diseases where oxidative stress contributes to pathology.

There’s life in the old dog yet: vitamin C as a therapeutic option in endothelial dysfunction.

Journal of Critical Care – August 2014 [http://www.ncbi.nlm.nih.gov/pubmed/25184406]

CONCLUSION:   In vitro and animal studies showed promising results and explained the impact of vitamin C, particularly in cases with endothelial disfunction. Indeed, studies using high-dose vitamin C and the parenteral route of application seem to be more successful than oral vitamin C delivery.

Effect of vitamin C on endothelial function in health and disease: a systematic review and meta-analysis of randomised controlled trials.

Atherosclerosis – July 2014 [http://www.ncbi.nlm.nih.gov/pubmed/24792921]

CONCLUSION:   Vitamin C supplementation improved endothelial function. The effect of vitamin C supplementation appeared to be dependent on health status, with stronger effects in those at higher cardiovascular disease risk.

Effects of vitamin C on health: a review of evidence.

Frontiers in bioscience (Landmark edition) – June 2013 [http://www.ncbi.nlm.nih.gov/pubmed/24217301]

CONCLUSION:   This review attempts to summarize recent and well established advances in vitamin C research and its clinical implications. Since vitamin C has the potential to counteract inflammation and subsequent oxidative damage that play a major role in the initiation and progression of several chronic and acute diseases, it represents a practical tool to administer for the early prevention of these pathologic conditions.

Inflammation in the vascular bed: importance of vitamin C.

Pharmacology & therapeutics – July 2008 [http://www.ncbi.nlm.nih.gov/pubmed/1852947]

CONCLUSION:   Although further studies of ascorbate function in these cell types and in novel animal models are needed, available evidence generally supports a salutary role for this vitamin in ameliorating the earliest stages of atherosclerosis.

Vitamin C supplementation lowers serum low-density lipoprotein cholesterol and triglycerides: a meta-analysis of 13 randomised controlled trials.

Journal of Chriporactic Medicine – June 2008 [http://www.ncbi.nlm.nih.gov/pubmed/19674720]

CONCLUSION:   Supplementation with at least 500 mg/d of vitamin C, for a minimum of 4 weeks, can result in significant decrease in serum LDL cholesterol and triglyceride concentrations.

Intra-arterial vitamin C prevents endothelial dysfunction caused by ischemia-reperfusion.

Atherosclerosis – March 2008 [http://www.ncbi.nlm.nih.gov/pubmed/17645881]

CONCLUSION:   Our data indicate that IR-induced vascular injury can be prevented by administration of antioxidants.

Effect of vitamin C on blood glucose, serum lipids & serum insulin in type 2 diabetes patients.

Indian Journal of Medical Research – November 2007 [http://www.ncbi.nlm.nih.gov/pubmed/18160753]

CONCLUSION:   Our results indicate that daily consumption of 1000 mg supplementary vitamin C may be beneficial in decreasing blood glucose and lipids in patients with type 2 diabetes and thus reducing the risk of complications.

Effect of ascorbic acid on prevention of hypercholesterolemia induced atherosclerosis.

Molecular and cellular biochemistry – April 2006 [http://www.ncbi.nlm.nih.gov/pubmed/16479321]

CONCLUSION:   This suggests that use of ascorbic acid may have great promise in the prevention of hypercholesterolemia induced atherosclerosis.

Vitamin C lowers blood pressure and alters vascular responsiveness in salt-induced hypertension.

Canadian journal of physiology and pharmacology – December 2002 [http://www.ncbi.nlm.nih.gov/pubmed/12564647]

CONCLUSION:   The results suggest that the antihypertensive effect of vitamin C is associated with a reduction in vascular sensitivity to noradrenaline and enhancement of endothelium-dependent relaxation due to increased nitric oxide bioavailability.

Vulnerable atherosclerotic plaque morphology in apolipoprotein E-deficient mice unable to make ascorbic Acid

Circulation – March 2002 [http://www.ncbi.nlm.nih.gov/pubmed/11914259]

CONCLUSION:   Chronic vitamin C deficiency does not influence the initiation or progression of atherosclerotic plaques but severely compromises collagen deposition and induces a type of plaque morphology that is potentially vulnerable to rupture.

Vitamin C inhibits endothelial cell apoptosis in congestive heart failure.

Circulation (AHA) – October 2001 [http://www.ncbi.nlm.nih.gov/pubmed/11684628]

CONCLUSION:   Administration of vitamin C to congestive heart failure patients suppresses endothelial cell apoptosis in vivo, which might contribute to the established functional benefit of vitamin C supplementation on endothelial function.

Hyperglycemia-induced ascorbic acid deficiency promotes endothelial dysfunction and the development of atherosclerosis.

Atherosclerosis – September 2001 [http://www.ncbi.nlm.nih.gov/pubmed/11500168]

CONCLUSION:   Vitamin C administration is recommended during periods of both acute and chronic hyperglycemia to help preserve endothelial function.

Vitamin C improves endothelium-dependent vasodilation by restoring nitric oxide activity in essential hypertension.

Atherosclerosis – September 2001 [http://www.ncbi.nlm.nih.gov/pubmed/9631871]

CONCLUSION:   In essential hypertensive patients, impaired endothelial vasodilation can be improved by the antioxidant vitamin C, an effect that can be reversed by the nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine. These findings support the hypothesis that nitric oxide inactivation by oxygen free radicals contributes to endothelial dysfunction in essential hypertension.

Vitamin C improves endothelial function of conduit arteries in patients with chronic heart failure.

Atherosclerosis – September 2001 [http://www.ncbi.nlm.nih.gov/pubmed/9468210]

CONCLUSION:  Vitamin C improves FDD in patients with CHF as the result of increased availability of nitric oxide. This observation supports the concept that endothelial dysfunction in patients with CHF is, at least in part, due to accelerated degradation of nitric oxide by radicals.

Ascorbic acid and atherosclerotic cardiovascular disease.

Sub-cellular biochemistry – 1996 [http://www.ncbi.nlm.nih.gov/pubmed/8821982]

CONCLUSION:  A particularly intriguing possible mechanism for the anti-atherogenic effect of vitamin C is prevention of atherogenic, oxidative modification of LDL. Numerous in vitro studies have demonstrated that ascorbic acid strongly inhibits LDL oxidation by a variety of mechanisms. The potential effects of ascorbic acid on platelet function and EDRF metabolism are particularly intriguing, as they might have widespread consequences for the prevention of atherosclerotic lesion development as well as acute clinical events. Thus, both metabolic and antioxidant functions may contribute to the possible reduction of CVD risk by vitamin C.

Hypothesis: lipoprotein(a) is a surrogate for ascorbate.

Proceedings of the National Academy of Sciences of the United States of America – August 1990 [http://www.ncbi.nlm.nih.gov/pubmed/2143582]

CONCLUSION:  The concept that lipoprotein(a) [Lp(a)] is a surrogate for ascorbate is suggested by the fact that this lipoprotein is found generally in the blood of primates and the guinea pig, which have lost the ability to synthesize ascorbate, but only rarely in the blood of other animals. Properties of Lp(a) that are shared with ascorbate, in accordance with this hypothesis, are the acceleration of wound healing and other cell-repair mechanisms, the strengthening of the extracellular matrix (e.g., in blood vessels), and the prevention of lipid peroxidation. High plasma Lp(a) is associated with coronary heart disease and other forms of atherosclerosis in humans, and the incidence of cardiovascular disease is decreased by elevated ascorbate. Similar observations have been made in cancer and diabetes. We have formulated the hypothesis that Lp(a) is a surrogate for ascorbate in humans and other species and have marshalled the evidence bearing on this hypothesis.

Modulation of the effects of ascorbic acid on lipid peroxidation by tocopherol in adrenocortical mitochondria.

Journal of steroid biochemistry – April 1989 [http://www.ncbi.nlm.nih.gov/pubmed/2724965]

CONCLUSION: The results indicate that the actions of AA are determined in part by mitochondrial tocopherol content and, as a result, vary in the different zones of the adrenal cortex.

Modulation of the effects of ascorbic acid on lipid peroxidation by tocopherol in adrenocortical mitochondria.Inhibition of HMG-CoA reductase activity by ascorbic acid. An effect mediated by free radical monodehydroascorbate.

Journal of Biological Chemistry – June 1986 [http://www.ncbi.nlm.nih.gov/pubmed/3711081]

CONCLUSION:  Since inhibition of HMG-CoA reductase occurs at physiological concentrations of ascorbic acid in the human leucocyte, this vitamin may be important in the regulation of endogenous cholesterol synthesis in man.

Inhibition of HMG-CoA reductase activity by ascorbic acid. An effect mediated by free radical monodehydroascorbate.

Journal of Biological Chemistry – June 1986 [http://www.ncbi.nlm.nih.gov/pubmed/3711081]

CONCLUSION: Since inhibition of HMG-CoA reductase occurs at physiological concentrations of ascorbic acid in the human leucocyte, this vitamin may be important in the regulation of endogenous cholesterol synthesis in man.

Effect of ascorbic acid on plasma cholesterol in humans in a long-term experiment.

International journal for vitamin and nutrition research – 1977 [http://www.ncbi.nlm.nih.gov/pubmed/881295]

CONCLUSION:  During the period of a low vitamin C intake (approximately equal to 20 mg per day) ascorbic acid in a dose of 2 x 500 mg per day was administered to 82 men and women aged 50-75 years. A correlation of plasma cholesterol levels determined before and after a three months’ administration of ascorbic acid showed the effect of vitamin C to be dependent on the starting concentration of plasma cholesterol: the higher the initial cholesterolemia, the greater the hypocholesterolemic effect of ascorbic acid. On restricting the experimental group to subjects with an initial cholesterolemia above 230 mg%, the effect of the same dose of ascorbic acid on cholesterolemia was followed in three-month periods for a further 9 months. In all these time intervals, ascorbic acid was found significantly to depress cholesterolemia and its effects persisted 6 weeks after termination of the experiment. The administration of 2 x 500 mg ascorbic acid daily during one year resulted in an abrupt increase of ascorbemia and a marked accumulation of ascorbic acid in the leucocytes. Six weeks following interruption of ascorbic acid intake, vitamin C concentration in the leucocytes significantly declined but still continued to be twice higher than in the control receiving no ascorbic acid supplement.

Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in Get With The Guidelines.

American heart journal – January 2009 [http://www.ncbi.nlm.nih.gov/pubmed/19081406]

CONCLUSION:  In a large cohort of patients hospitalized with CAD, almost half have admission LDL levels <100 mg/dL (2.6 mmol/L). More than half the patients have admission HDL levels <40 mg/dL (1.0 mmo/L), whereas <10% have HDL > or =60 mg/dL (1.5 mmol/L).

Lipid-lowering therapy and cholesterol levels following acute myocardial infarction: a German study of 5361 patients.

European journal of epidemiology – 2003 [http://www.ncbi.nlm.nih.gov/pubmed/881295]

CONCLUSION:  The range of TC values of the patients examined was comparable to those in the CARE and the 4S secondary prevention studies. It can therefore be assumed that the results of these studies are also applicable to Germany. Nevertheless, according to existing data, therapy with lipid-lowering drugs is currently unsatisfactory, even in secondary prevention.

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