CURCUMIN (BCM-95® - Very High Absorb | Retention) REFERENCES
Curcumin provides extensive coverage for the strengthening and protection of the cardiovascular system. The prolific nature of curcumin’s benefits extend anti-aging effects to the vascular system, helping to ameliorate pathological changes to the arteries, including the initiation and progression of atheroscleosis. Curcumin also helps protect the heart and laboratory studies suggest that curcumin may lessen the potential for cardiac hypertrophy and heart failure.(13) Furthermore curcumin possesses anti-thrombotic properties, which helps in the prevention of abnormal platelet aggregation and possible clot formation.
Until recently, using curcumin as a dietary supplement has been problematic due to its low bioavailability. Curcumin extract is very poorly absorbed by the body, which minimizes its potential usefulness and effectiveness. However, advances in research now provide a next generation form of curcumin, which is both highly absorbed and maintained by the body. BCM-95® curcumin is a special curcuminoid complex which circumvents these problems by delivering maximum absorption (7X’s more absorption) with longer retention (4 hours more) in the blood stream as compared to normal curcumin 95% extract. (16)
Cardiovascular Research Benefits:
Cardiovascular Anti-Aging: Lowering Key Aging Risk Factors
- Inhibits the over stimulation of the inflammatory response which accelerates aging and is associated with acute and chronic diseases (including cardiovascular disease).(14)
- Inhibits the proliferation of vascular smooth muscle cells. The proliferation of vascular smooth muscle cells increases arterial wall thickness and is associated with cardiovascular aging and arteriosclerosis.(15).
Inflammation and C-Reactive Protein:
- Reduces Systemic Inflammation.Curcumin inhibits High mobility group box 1 (HMGB1) proteins, which are a powerful mediator of inflammation, and is believed responsible for atherosclerotic plaque development.(33,34) Curcumin further supresses the inflammation stimulating transcription factor NF-kappaB. NF-kappaB operates at the gene level, and activates the genes responsible for the inflammatory response.(16, 18. 19) Also inhibits inflammatory enzymes COX-2 and 5-LOX and cytokines including TNF (tumor necrosis factor), and interleukin 6.(5)
- Inhibits Inflammatory Mediators from Fat Cells (Adipocytes). Low grade, chronic inflammation is produced by adipocytes, and is especially evident is obese individuals. Curcumin suppresses the inflammation generated by the adipose tissue. As the researchers note, inflammation from adipocytes has been linked to cardiovascular disease and to insulin resistance.(17)
- Reduces C-reactive protein (CRP) levels. CRP, being a marker of inflammation (as well as a direct contributor to cardiovascular disease development), is reduced as corresponding systemic levels of inflammation are reduced by curcumin.
- Anti-Thrombic and Healthy Platelet Activity.
Helps to inhibit platelet aggregation which can increase the risk of clotting.(20)
Healthy Endothelium & Vascular Functioning
- Prevents Oxidation and Lipid Modification of LDL. Oxidized LDL inflicting damage to the arterial wall is an important step in the progression of atherosclerosis. Curcumin both prevents LDL oxidation and also prevents oxidized LDL inhibition of as an important molecule synthesized by the endothelial lining. This molecule, prostacyclin, is an effective vasodilator, and also plays an important role in preventing the formation of blood clots. Researchers conclude that “Curcumin supplementation could be an effective strategy in preventing LDL oxidation and its impact on atherosclerosis and lesion formation.”(21)
- Increases HDL “Good Cholesterol” levels and Paraoxonase (PON) Activity. HDL is involved with the removal of cholesterol from atherosclerotic arteries and returns the cholesterol to the liver for excretion. High levels of HDL are known as being protective against the development of atherosclerosis. PON1 (Paraoxonase 1), is synthesized in the liver and works in conjunction with HDL. Specifically, PON1 inhibits the formation of the oxidized-LDL found in atherosclerotic plaques. In studies with lab animals, curcumin increased plasma HDL and paraoxonase activity.(31)
- Protective and Therapeutic Reversal of Vascular Dysfunction.
o Oxidative Stress Induced Dysfunction. Laboratory animals administered an endotoxin (a substance which elicits a strong inflammatory response by the immune system and increased levels of oxidative stress), experienced impairment to the vascular system, including the heart and vascular responsiveness. Curcumin (administered both before and after the toxin), both prevented the on-set of dysfunction, and also provided therapeutic normalization.(22)
o High Glucose Induced Dysfunction. High glucose levels (which are especially seen in diabetics and pre-diabetics), result in an endothelial vasodilation dysfunction. When curcumin was incubated together with high glucose medium, vascular dysfunction showed reversal.(23)
o Increases Secretion of Adiponectin by Adipocyte (Fat) Tissue | Aids in Protection of the Endothelium from Dysfunction. Adiponectin is a protein which is secreted only by adipose tissue. Involved in metabolic processes in the body, adiponenctin is thought to play important roles in lipid metabolism and cardiovascular disease.(24) Adiponectin is considered as being anti-diabetic and anti-atherogenic.(25) Among the metabolic actions of adiponectin includes aiding in glucose uptake (enhancing insulin sensitivity), the clearing of triglycerides from the bloodstream, lowering LDL, increasing HDL levels and protection of the vascular endothelium against dysfunction. Research studies show that curcumin both increases adiponectin secretion, and also decreases levels of inflammatory interleukin-6 (IL-6) secretion.(26)
Inhibition of Cardio Hypertrophy and Heart Failure
- Inhibits p300 Histone Acetyltransferase (HAT) Activity. Curcumin is known as a “p300” blocker (27), and has been shown in laboratory studies to prevent the hypertrophy and heart failure in research animals.
- Cardiac hypertrophy (hypertrophy of the cardiomyocytes) and subsequent heart failure is associated with P300 HAT activity. Using rats as the experimental animal, it has been demonstrated that curcumin effectively suppresses P300 HAT activity and heart hypertrophy.The study involved the use of two heart failure models:
- Hypertensive Heart Disease (using salt sensitive rats)
- Myocardial Infarction (using surgically manipulated rats)
In each of these instances, curcumin was able to block an increase in the thickness of the myocardial wall, and decreases in systolic functioning.(28) Authors of the study conclude that “inhibition of p300 HAT activity by the nontoxic dietary compound curcumin may provide a novel therapeutic strategy for heart failure in humans.”
- Diabetic Cardiomyopathy. Another instance of cardiac hypertrophy occurs in diabetes, resulting in a condition known as diabetic cardiomyopathy. Diabetes cardiomyopathy is a serious condition that eventually leads to heart failure. Like other pathological conditions resulting in cardiac hypertrophy, P300 activity is a significant event in diabetic hypertrophy development. Research with glucose incubated rat cardiomyocytes, showed molecular markers of cardio hypertrophy. Treatment with curcumin was shown to block p300 activity and the same markers associated with cardio hypertrophy. (29)
Cardioprotective via Altered Gene Expression in Myocardial Infarction
- Myocardial Infarction (also known as heart attack) is the term used to describe the interruption of blood supply to the heart. As a result, oxygen does not reach parts of the heart and heart muscle cells die (known as infraction). Commonly the outcome of a myocardial infarction is the loss of heart functional capacity.
- Curcumin improves cardiovascular function and reverse some abnormal changes in experimentally induced myocardial infraction. Conducted using rat models, curcumin given after a myocardial infraction was shown to improve cardiovascular function and diminish the area of the myocardial cell death (infract area). Researchers conclude that curcumin provides cardioprotective effects through the positive alteration of gene expression in the heart muscle.(30)
- Munk PS, et al. Inflammation and C-reactive protein in cardiovascular disease. Tidsskr Nor Laegeforen. 2009 Jun 11;129(12):1221-4.
- Bispendial RJ, et al. C-reactive protein elicits white blood cell activation in humans. Am J Med. 2009 Jun;122(6):582.e1-9.
- Antony, B. et al. A Pilot Clinical Study to Evaluate the effect of Emblica Officialis Extract (AmlaMaxTM) on Markers of Systemic Inflammation and Dyslipidia. Indian Journal of Clinical Biochemistry, 2008 / 23 (4) 378-381
- Yokozawa T, et al. Amla (Emblica officinalis Gaertn.) prevents dyslipidaemia and oxidative stress in the ageing process. Br J Nutr. 2007 Jun;97(6):1187-95.
- Aggarwal BB, et al. Pharmacological basis for the role of curcumin in chronic diseases: an age-old spice with modern targets. Trends Pharmacol Sci. 2009 Feb;30(2):85-94.
- Almozning-Sarafian D, et al. Magnesium and C-reactive protein in heart failure: an anti-inflammatory effect of magnesium administration? Eur J Nutr. 2007 Jun;45(4):230-7
- King JL, et al. Inadequate dietary magnesium intake increases atherosclerotic plaque development in rabbits. Nutr Res. 2009 May;29(5):343-9
- Antony B, et al. A Pilot Clinical Study to Evaluate the Effect of Emblica Officinalis Extract (AmlaMax™) on Markers of Systemic Inflammation and Dyslipidemia. Indian Journal of Clinical Biochemistry, 2008 / 23 (4) 378-38
- Rajak S, et al. Emblica officinalis causes myocardial adaptation and protects against oxidative stress in ischemic reperfusion injury in rats. Phytother Res. 2004 Jan;18(1):54-6
- Kim HJ, et al. Influence of amla (Emblica officinalis Gaertn.) on hypercholesterolemia and lipid peroxidation in cholesterol-fed rats. J Nutr Sci Vitaminol (Tokyo). 2005 Dec;51(6):413-8
- Yokozawa T, et al. Amla (Emblica officinalis Gaertn.) prevents dyslipidaemia and oxidative stress in the aging process, Br J Nutr. 2007 Jun;97(6):1187-95
- Rao TP, et al. Amla (Embilca officinalis Gaertn.) extracts reduce oxidative stress in streptozotocin-induced diabetic rats. J Med Food. 2005 Fall;8(3):362-8
- Womgcharoen W, et al. The protective role of curcumin in cardiovascular diseases. Int J Cardiol. 2009 Apr 3;133(2):145-51
- Bengmark S. Curcumin, an atoxic antioxidant and natural NFkappaB, cyclooxygenase-2, lipooxygenase, and inducible nitric oxide synthase inhibitor: a shield against acute and chronic diseases. JPEN J Parenter ENteral Nutr. 2006 Jan-Feb;30(1):45-51
- Oin L, et al. Effects and underlying mechanisms of curcumin on the proliferation of vascular smooth muscle cells induced by Chol:MbetaCD. Biochem Biophys Res Commun. 2009 Feb 6;379(2):277-82
- Antony B, et al. A Pilot Cross-Over Study to Evaluate Human Oral Bioavailability of BCM-95® CG (BiocurcuminTM). A Novel Bioenhanced Preparation of Curcumin. Indian J. Pharm. Sci, 2008, 70(4)
- Gonzales AM, et al. Curcumin and resveratrol inhibit nuclear factor-kappaB-mediated cytokine expression in adipocytes, Nutr Metab (Lond). 2008 Jun 12;5:17.
- Menon VP, et al. Antioxidant and ant-inflammatory properties of curcumin. Adv Exp Med Biol. 2007;595:105-25.
- Jagetia GC, et al. “Spicing up” of the immune system by curcumin. J Clin Immunol. 2007 Jan;27(1):19-35
- Srivastava KC, et al. Curcumin, a major component of food spice turmeric (Curcuma longa) inhibits aggregation and alters eicosanoid metabolism in human blood platelets. Prostaglandins Leukot Essent Fatty Acids. 1995 Apr;52(4):223-7.
- Mahfouz MM, et al. Curcumin prevents the oxidation and lipid modification of LDL and its inhibition of prostacyclin generation by endothelial cells in culture. Prostaglandins Other Lipid Mediat. 2009 Jun 20.
- Samoamit K, et al. Curcumin improves vascular function and alleviates oxidative stress in non-lethal lipopolysaccharide-induced endotoxaemia in mice. Eur J Pharmacol. 2009 Jun 17
- Fang XD, et al. Curcumin ameliorates high glucose-induced vascular endothelial dysfunction in rat thoracic aorta. Clin Exp Pharmacol Physiol. 2009 May 19.
- Lara-Castro C, et al. Adiponectin and the metabolic syndrome: mechanisms mediating risk for metabolic and cardiovascular disease. Curr Opin Lipidol. 2007 Jun;18(3):263-70.
- Kralisch S, et al. Adiokines in diabetes and cardiovascular diseases. Minerva Endocrinol. 2007 Sep;32(3):161-71.
- Ou XB, et al. Effects of curcumin on secretion of adiponectin and interleukin-6 in human adipose tissues: an in vitro study. Zhong Xi Yi Jie He Xue Bao. 2008 Jul;6(7):711-5.
- Marcu MG, et al. Curcumin is an inhibitor of p300 histone acetylatransferase. Med Chem. 2006 Mar;2(2):169-74.
- Morimoto T, et al. The dietary compound curcumin inhibits p300 histone acetyltransferase activity and prevents heart failure in rats. J Clin Invest. 2008 Mar;118(3):868-78
- Feng B, et al. Regulation of cardiomyocyte hypertrophy in diabetes at the transcriptional level. Am J Physiol Endocrinol Metab. 2008 Jun;294(6):E1119-26.
- Hong D, et al. Altered profiles of gene expression in curcumin-treated rats with experimentally induced myocardial infarction. Pharmacol Res. 2009 Sep 9.
- Jang EM, et al. Beneficial effects of curcumin in hyperlipidemia and insulin resistance in high-fat-fed hamsters. Metabolism. 2008 Nov;57(11):1576-83.
- King DE. Inflammation and elevation of C-reactive protein: Does magnesium play a key role? Magnes Res. 2009 Jun;22(2):57-9.
- de Souza AW,et al. HMGB1 in vascular diseases: Its role in vascular inflammation and atherosclerosis. Autoimmune Rev. 2012 Oct;11(12):909-17.
- Kim DC, et al. Vascular anti-inflammatory effects of curcumin on HMGB1-mediated responses in vitro. Inflamm Res. 2011 Dec;60(12):1161-8