Compiled by Barbara Connor, M.Ac., L.Ac.
Table of Contents
Introduction
Natural Compounds that Reduce the Risk of Heart Attacks or Benefit Heart Health
Benefits of Exercise & Life Style Changes in Reducing the Risk of Heart Attacks or Heart Disease
Cholesterol, Statins and Heart Disease
Natural Compounds Which Can Be Used to Reduce the Dependency on Statins
Natural Compounds Which Can Help to Lower Blood Pressure
Introduction
There is growing consensus that systemic inflammation is at the heart of cardiovascular disease (CVD). Inflammation is a key feature of the immune system, functioning to defend tissue integrity and function. However, chronic stimulation of inflammatory mediators leads to lasting vascular reactivity, insulin resistance, hyperlipidemia, and, subsequently, chronic disease. Dietary practices to minimize inflammatory stimuli and CVD risk include regular intakes of fatty fish rich in the eicosapentaenoic and docosahexaenoic acids that compete with the more pervasive membrane fatty acid, arachidonic acid, disrupting the metabolic cascades that stimulate inflammation. (Johnston C 2009)
Since oxidative stress plays a prominent role in immune system activation, regular ingestion of ample amounts of fruits and vegetables (8+ servings/d) rich in antioxidant compounds, the polyphenols, carotenoids, and vitamin C (e.g., citrus, tomatoes, berries, carrots, and greens), lowers inflammatory mediators and risk for chronic disease. Whole grains, legumes, and nuts have also been demonstrated in clinical trials to effectively reduce inflammatory mediators and risk for CVD. (Johnston C 2009)
Mediterranean-style diet – Higher consumption of a Mediterranean-style diet was associated with decreased risk of vascular events. Results support the role of a diet rich in fruit, vegetables, whole grains, fish, and olive oil in the promotion of ideal cardiovascular health. (Gardener et al 2011)
Nuts and soy, a high ratio of white to red meat, a high intake of fiber, and moderate alcohol – Our findings emphasize the importance of a high intake of nuts and soy, a high ratio of white to red meat, a high intake of fiber, and moderate alcohol intake in the decrease of all-cause mortality. (Akbaraly et al 2011)
Fish, poultry, dairy products, and especially nuts – In a large study of 84,136 U.S. women, it was found that greater consumption of red meat was associated with a higher risk of coronary heart disease. Compared to the same number of servings of red meat, consumption of fish, poultry, dairy products, and especially nuts was associated with lower risk. These finding suggest that the risk of coronary heart disease may be reduced importantly by shifting the sources of protein in the U.S. diet. (Bernstein et al 2010)
Antioxidants (found in cranberries, blueberries, raspberries, blackberries, beans, artichokes, Russet potatoes, walnuts and hazelnuts) – Various reports suggest that antioxidant therapy after ischemia/reperfusion (I/R) would help the myocardium to recover from reactive oxygen species (ROS)-induced damage. The deleterious effects of ROS on cardiac tissue can be blocked by antioxidant enzymes such as superoxide dismutase and catalase. These studies indicated that antioxidants capable of scavenging ROS, including reactive oxygen free radicals such as superoxide, hydroxyl, and peroxyl radicals, could have therapeutic advantages to treat I/R-mediated cardiac injury. (Swaminathan et al 2010)
Isolated soy protein diet – The ISP (isolated soy protein) diet was able to improve ventricular systolic and diastolic function in the groups IS<25% and IS>25% (left ventricular end diastolic pressure was reduced by 44% and 24%, respectively) and to decrease myocardial oxidative stress. The overall results confirm the preventive role of soy-derived products in terms of post-MI myocardial dysfunction probably by an antioxidant action. (Hagen et al 2009)
Reduce hyperglycemia (high blood sugar). Hyperglycemia on admission to the hospital is associated with increased mortality rates in patients with ST-elevation myocardial infarction (STEMI). (Eitel et al 2012)
The intake of wholegrain foods clearly protects against heart disease and stroke. (Flight & Clifton 2006)
Oatmeal – Seven of the eight studies reported lower total and low density lipoproteins (LDL) cholesterol with oatmeal foods than control foods. When the studies were combined in a meta-analysis lower total cholesterol (-0.20 mmol/L, 95% confidence interval (CI) -0.31 to -0.10, P = 0.0001 ) and LDL cholesterol (0.18 mmol/L, 95% CI -0.28 to -0.09, P < 0.0001) were found with oatmeal foods. However, there is a lack of studies on other wholegrains or wholegrain diets. (Kelly et al 2007 Cochrane Database Syt Rev.)
Omega-3 polyunsaturated fatty acids – are found in fish oil and they have been shown to mitigate the risk of cardiovascular disease. They reduce fatal and nonfatal myocardial infarction, stroke, coronary artery disease, sudden cardiac death, and all-cause mortality. They also have beneficial effects in mortality reduction after a myocardial infarction. Omega-3 fatty acids have also been shown to have beneficial effects on arrhythmias, inflammation, and heart failure. They may also decrease platelet aggregation and induce vasodilation. Omega-3 fatty acids also reduce atherosclerotic plaque formation and stabilize plaques preventing plaque rupture leading to acute coronary syndrome. Moreover, omega-3 fatty acids may have antioxidant properties that improve endothelial function and may contribute to its antiatherosclerotic benefits. (Kar S 2011)
DHA & EPA – The most compelling evidence for the cardiovascular benefit provided by omega-3 fatty acids comes from 3 large controlled trials of 32,000 participants randomized to receive omega-3 fatty acid supplements containing docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) or to act as controls. These trials showed reductions in cardiovascular events of 19% to 45%. These findings suggest that intake of omega-3 fatty acids, whether from dietary sources or fish oil supplements, should be increased, especially in those with or at risk for coronary artery disease. Patients should consume both DHA and EPA. (Lee et al 2008)
Cilantro (coriander) – Our results show that methanolic extract of CS (Coriandrum sativum L.) is able to prevent myocardial infarction by inhibiting myofibrillar damage. It is also concluded that, the rich polyphenolic content of CS extract is responsible for preventing oxidative damage by effectively scavenging the Isoproterenol generated ROS. (Patel et al 2012)
Spices – are rich in antioxidants, and scientific studies suggest that they are also potent inhibitors of tissue damage and inflammation caused by high levels of blood sugar and circulating lipids. (Vasanthi & Parameswari 2010)
Avoid partially hydrogenated vegetable oil – The fatty acids in partially hydrogenated vegetable oil are 14 cis and trans isomers of octadecenoic and octadecadienoic acids that are formed during hydrogenation. They causeinflammation and calcification of arterial cells: known risk factors for coronary heart disease (CHD). (Kummerow FA 2009)
Avoid trans fatty acids (TFA) – A meta-analysis of prospective studies indicated 24, 20, 27 and 32% higher risk ofmyocardial infarction (MI) or coronary heart disease death for every 2% energy of TFA consumption isocalorically replacing carbohydrate, saturated fatty acids (SFA), cis monounsaturated fatty acids and cis polyunsaturated fatty acids, respectively. (Mozaffarian et al 2009)
Natural Compounds that Reduce the Risk of Heart Attacks or Benefit Heart Health
Alpha-lipoic acid (ALA) was originally identified as an obligatory cofactor for mitochondrial α-ketoacid dehydrogenases and was found to play an important role in mitochondrial energy metabolism. ALA enhances glucose utilization in isolated rat hearts. Growing evidence suggests that ALA maintains the cellular antioxidant status by either enhancing or inducing the uptake of antioxidant enzymes. ALA administration reduces aortic AGEs (advanced glycation end-products) content, cardiac mitochondrial superoxide production, and insulin resistance in diabetic animal models. (Lee et al 2012)
Alpha-lipoic acid – Administration of lipoic acid significantly up-regulated cellular ALDH2 activity concomitantly with a reduction in apoptosis, production of reactive oxygen species, 4-HNE and MDA, these effects were reversed in the presence of ALDH2 or PKCε inhibitors. Our results suggest that the cardioprotective effects of lipoic acid onischemia-reperfusion injury are through a mechanism involving ALDH2 activation. The regulatory effect of lipoic acid on ALDH2 activity is dependent on PKCε signaling pathway. (He et al 2012)
Andrographis paniculata – Present studies on Andrographis paniculata concentrate on Andrographolide and the flavonoid component API0134. This flavonoid component API0134 could improve canine heart function, decrease the extent of myocardial infarcted area, alleviate the extent of myocardial injury, and decrease the occurrence of arrhythmias. (Yuan & Jing 2011)
Angelica sinensis extract may improve anti-oxidant capacity, activate ERK signaling transduction pathway, and enhance the expression of endothelial NOS. Radix angelica sinensis could upregulate the expression of Bcl-2 and downregulate the expression of Bax, causing a decreased Bax/Bcl-2 ratio, so that apoptosis of the myocytes could be inhibited, and left ventricular function and ventricular remodeling improved. (Shangguan et al 2008)
Arjuna – Many experimental studies have reported its antioxidant, anti-ischemic, antihypertensive, and antihypertrophic effects, which have relevance to its therapeutic potential in cardiovascular diseases in humans. Several clinical studies have reported its efficacy mostly in patients with ischemic heart disease, hypertension, and heart failure. (Maulik & Talwar 2012)
Arjuna – Experimental studies have revealed the bark of Terminalia arjuna Wight & Arn exerting significant inotropic and hypotensive effect, increasing coronary artery flow and protecting myocardium against ischemic damage. It has also been detected to have mild diuretic, antithrombotic, prostaglandin E(2) enhancing and hypolipidaemic activity. There is ample clinical evidence of its beneficial effect in coronary artery disease alone and along with statin. (Dwivedi S 2007)
Astragalus – Total flavonoids of Astragulus and Astragaloside A work as inotropic agents by way of increasing cAMP contents of the myocardium, and inhibiting the activity of the Na+-K+-ATPase on the myocardial cellular membrane, while Astragalosides act as free radical scavengers. Astragaloside IV is a leading active ingredient with inotropic effect, not only improving heart function of the experimental rats, but also avoiding an increase of the oxygen consumption of the myocardium. (Yuan & Jing 2011)
Bacopa monniera — Histopathological studies and myocardial creatine phosphokinase content further confirmed the cardioprotective effects of B. monniera in the experimental model of ischaemia-reperfusion injury. The study provides scientific basis for the putative therapeutic effect of B. monniera in ischaemic heart disease. Interestingly, B. monniera also restored the antioxidant network of the myocardium and reduced myocardial apoptosis, caspase 3 and Bax protein expression. (Mohanty et al 2010)
Baicalin is a flavonoid compound extracted from Scutellaria baicalensis Georgi. Baicalin significantly improved the SOD activity of the hypoxic myocytes of neonatal Sprague-Dawley rats inhibited NO secretion. When baicalin was given to the rats 5 mins before ligation of the coronary artery, the post-infarction heart function improved with decreased malondialdehyde content and increased SOD activity (Liu et al 2003).
Berberine (goldenseal) – had positive inotropic action and improved heart function of heart failure patients. (Cui 2006)
Carnitine, taurine and coenzyme Q(10) – Our results support the potential cardioprotective impact of carnitine, taurine and coenzyme Q(10) during myocardial ischemia. In contrast to carnitine supplementation alone, carnitine, taurine and coenzyme Q(10) improved survival as well as cardiac function, gene expression and delayed remodeling. (Briet et al 2008)
Coenzyme Q(10) (CoQ(10) – Patients with chronic heart failure have low plasma concentrations of CoQ(10), an essential cofactor for mitochondrial electron transport and myocardial energy supply. Additionally, low plasma total cholesterol (TC) concentrations have been associated with higher mortality in heart failure. Plasma CoQ(10) is closely associated with low-density lipoprotein cholesterol (LDL-C), which might contribute to this association. (Molyneux et al 2008)
Coenzyme Q(10) – Long-term treatment with ubiquinone increases plasma and myocardial CoQ content and this can improve the survival of myocardial cells during ischemia and limit postinfarct myocardial remodeling.(Kalenikova et al 2007)
Coenzyme Q(10) – appears to be involved in the coordinated regulation between oxidative stress and antioxidant capacity of heart tissue. When the heart is subjected to oxidative stress in various pathogenic conditions, the amount of CoQ10 is decreased, which triggers a signal for increased CoQ10 synthesis. It has been reported that in patients with cardiac disease such as chronic heart failure, the myocardium becomes deficient in CoQ10and CoQ10reductase. CoQ10 level is also reduced in other cardiovascular diseases such as cardiomyopathy. CoQ10 can protect human low-density lipoprotein (LDL) from lipid peroxidation, suggesting its role in atherosclerosis. Several reports exist in the literature indicating cardioprotective effects of CoQ10 against ischemia-reperfusion injury. (Maulik et al 2000)
Coenzyme Q(10) – (1) Serum and myocardial levels of CoQ can be raised acutely by iv liposomal CoQ. (2) Myocardial CoQ levels correlate best with I/R (ischemia and reperfusion) protection. (3) Acute iv CoQ improves function and efficiency and decreases oxidant injury after I/R. Intravenous CoQ may be effective clinically for acute cardiac ischemic syndromes. (Niibori et al 1998)
Creatine – A large amount of experimental evidence shows that pretreatment with Creatine is capable of reducing the damage induced by ischemia or anoxia in both heart and brain, and that such treatment may also be useful even after stroke or myocardial infarction has already occurred. (Perasso et al 2011)
Curcuma longa (Turmeric) – In the present investigation it was observed that subsequent to ischemia and reperfusion injury, Curcuma longa treated group demonstrated significant anti-apoptotic property, which might contribute to the observed preservation in cardiac function and cardioprotective effects. Furthermore, the myocardial salvaging effects of Curcuma longa were supported by histopathological studies. (Mohanty et al 2006)
Curcumin, an inhibitor of NF-kappaB, ameliorated the surge of pro-inflammatory cytokines during cardiopulmonary bypass and decreased the occurrence of cardiomyocytic apoptosis after global cardiacischemia/reperfusion injury. (Yeh et al 2005)
Dan-Shen-Yin (DSY) – is a traditional Chinese formula comprising Salvia Miltiorrhiza, Sandalwood and Fructus Amomi. The results of this study show that DSY exerts significant cardioprotective effects against acute ischemic myocardial injury in rats, possibly through its anti-inflammatory and anti-oxidant properties, and may thus be used as a potential therapeutic reagent for the treatment of coronary heart disease. (Yan et al 2012)
EGCG (epigallocatechin-3-gallate) – the results of our study shows that EGCG protects the lysosomal membrane against ISO-induced cardiac damage. The observed effects might be due to the free radical scavenging and membrane stabilizing properties of EGCG. (Devika & Prince 2008)
Ginkgo biloba extract (Egb761) – has shown an antagonistic action on platelet-activating factor, a key point ofmyocardial injury. (Zhang and Gao, 2008).
Ginseng — Radix Ginseng is from Panax Ginseng, a herbaceous plant of the Araliaceae. The chemical components include ginsenosides, ginseng polysaccharides, and active peptides, etc. Ginsenosides can limit myocardial infarction size, regulate metabolism of arachidonic acid, and increase the 6-Keto-PGF1α/TXB2 ratio (Li et al 2006).
The optimal concentration of ginsenosides for myocardial protection was 20–80 mg/L, however, this drug may show a harmful effect on the myocardium when the concentration was 160 mg/L (Chen et al 1994). (Yuan et al 1997) obtained a similar result in a cardiac concordant xenotransplantation rat model where the proper concentration of the drug was 40 mg/L; whereas the protective effect diminished and it may jeopardize the myocardium when the concentration was 320 mg/L. (Yuan & Jing 2011)
Grape seed proanthocyanidins extract – The study suggests that grape seed proanthocyanidins extracts (GSPE) has a protective effect on myocardial ischemic reperfusion arrhythmias, which may be mediated by inhibiting the degradation of connexin 43 (Cx43) and enhancing gap junctional conductance. (Liang et al 2009)
Grape seed proanthocyanidins – have cardioprotective effects against reperfusion-induced injury via their ability to reduce or remove, directly or indirectly, free radicals in myocardium that is reperfused after ischemia. (Pataki et al 2002)
Hawthorn – The study confirms the protective effect of alcoholic extract of the berries of Crataegus oxyacantha against isoproterenol-induced inflammation and apoptosis-associated myocardial infarction in rats. (Vijayan et al 2012)
Hawthorn – The results suggested that Crataegus oxycantha extract attenuated apoptotic incidence in the experimental myocardial ischemia-reperfusion model by regulating Akt and HIF-1 signaling pathways. (Jayachandran et al 2010)
Hawthorn – Several studies have shown that Crataegus oxycantha (COC) extract is effective in quenching ROS, particularly free radicals. Human subjects treated with COC extract after myocardial infarction have shown improvements in heart rate, reduction in blood pressure, and an increase in the left-ventricular ejection volume. Moreover, meta analysis of a randomized trial with COC extract showed its beneficial role as an adjunctive treatment for chronic heart failure. The results of this study suggested that the COC extract may reduce the oxidative stress in the reperfused myocardium, and play a significant role in the inhibition of apoptotic pathways leading to cardioprotection. (Swaminathan et al 2010)
L-arginine and L-lysine – The protective effect of L-arginine and L-lysine on lysosomal enzymes and membrane bound ATPases was examined on isoproterenol induced myocardial infarction in rats. Lysosomal enzymes play an important role in the inflammatory process. The rats given isoproterenol intraperitoneally for 2 days showed significant changes in the marker enzymes, lysosomal enzymes and membrane bound phosphatases. Histopathological studies also confirmed the induction of myocardial infarction in isoproterenol administered rats. Prior oral treatment with L-arginine (250 mg kg(-1) daily) and L-lysine (5 mg kg(-1) daily) for 5 days significantly prevented these alterations and restored the enzyme activities to near normal. These findings demonstrate the protective effect of L-arginine and L-lysine in combination against isoproterenol induced cardiac damage. (Ebenezar et al 2003)
L-Carnitine – treatment initiated early after acute myocardial infarction and continued for 12 months can attenuate left ventricular dilation during the first year after an acute myocardial infarction, resulting in smaller left ventricular volumes at 3, 6 and 12 months after the emergent event. (Iliceto et al 1995)
Magnesium – Mg++ is beneficial in acute Myocardial Infarction, protection during open heart surgery and treatment and prevention of heart rhythm disturbances. (Akhtar et al 2011)
Magnesium – Hypomagnesemia is common in hospitalized patients, especially in the elderly with coronary artery disease (CAD) and/or those with chronic heart failure. Hypomagnesemia is associated with an increased incidence of diabetes mellitus, metabolic syndrome, mortality rate from CAD and all causes. Magnesium supplementation improves myocardial metabolism, inhibits calcium accumulation and myocardial cell death; it improves vascular tone, peripheral vascular resistance, afterload and cardiac output, reduces cardiac arrhythmias and improves lipid metabolism. Magnesium also reduces vulnerability to oxygen-derived free radicals, improves human endothelial function and inhibits platelet function, including platelet aggregation and adhesion, which potentially gives magnesium physiologic and natural effects similar to adenosine-diphosphate inhibitors such as clopidogrel. The data regarding its use in patients with acute myocardial infarction (AMI) is conflicting. Although some previous, relatively small randomized clinical trials demonstrated a remarkable reduction in mortality when administered to relatively high risk AMI patients, two recently published large-scale randomized clinical trials failed to show any advantage of intravenous magnesium over placebo. Nevertheless, there are theoretical potential benefits of magnesium supplementation as a cardioprotective agent in CAD patients, as well as promising results from previous work in animal and humans. These studies are cost effective, easy to handle and are relatively free of adverse effects, which gives magnesium a role in treating CAD patients, especially high-risk groups such as CAD patients with heart failure, the elderly and hospitalized patients with hypomagnesemia. Furthermore, magnesium therapy is indicated in life-threatening ventricular arrhythmias such as Torsades de Pointes and intractable ventricular tachycardia. (Shechter M 2010)
Olive leaf extract – In vitro, oleuropein and its major metabolite, hydroxytyrosol (which are polyphenols contained in olive leaf extract), exhibited a range of pharmacological properties beneficial for the cardiovascular system. These actions included enhanced nitric oxide production by mouse macrophages, antiinflammatory effects,protection against oxidative myocardial injury induced by ischemia and reperfusion, decreased blood pressure, inhibition of platelet aggregation and eicosanoid production, and scavenging of free radicals in addition to inhibition of 5- and 12-lipoxygenases . Oleuropein reduced infarct size, plasma lipid concentrations, and plasma markers of oxidative stress in cholesterol-fed rabbits. In vivo, olive leaf extract lowered blood cholesterol and lipid concentrations in cholesterol-fed rats and lowered blood pressure in nitro-L-arginine methyl ester-induced hypertensive rats as well as in normotensive rats. (Poudyal et al 2010)
N-acetyl cysteine (NAC) – Pretreatment with NAC showed protective effects on adenosine triphosphatases, minerals, and lipid peroxidation. The in vitro study confirmed the reducing property of NAC. The observed effects are due to the membrane-stabilizing and antioxidant effects of NAC. The results of this study will be useful for the prevention of myocardial infarction. (Meeran & Prince 2012)
N-3 PUFAs (n-3 polyunsaturated fatty acids) – Low levels of circulating n-3 PUFA are associated with decreased HF-free survival in post-acute myocardial infarction patients. (Hara et al 2012)
N-3 PUFAs – These results demonstrate that the increase in the dietary omega-3 PUFA, at the expense of omega-6 PUFA, reduces infarct size and helps to inhibit apoptosis in the limbic system after myocardial infarction in the rat. (Rondeau et al 2011)
N-3 PUFAs or probiotics – These results indicate that a high-PUFA n-3 diet or the administration of probiotics, starting after the onset of reperfusion, are beneficial to attenuate apoptosis in the limbic system and post-myocardial infarction depression in the rat. (Gilbert et al 2012)
N-3 PUFAs – A beneficial role of fish consumption on the risk of myocardial infarction (MI) has been reported and is mostly ascribed to n-3 (omega-3) fatty acids. The biomarker results indicate a protective effect of fish consumption. No harmful effect of mercury was indicated in this low-exposed population in whom Ery-Hg and P-EPA+DHA were intercorrelated. (Wennberg et al 2011)
N-3 PUFAs – Treatment with n-3 fatty acids after myocardial infarction exerts favorable effects on levels of platelet- and monocyte-derived microparticles, thus possibly explaining some of the anti-inflammatory and anti-thrombotic properties of these natural compounds. (Del Turco et al 2008)
Panax Notoginseng saponins could improve the Ca2+ pump activity on the membranes of myocardial sarcoplasmic reticulum, reduce myocardial intracellular Ca2+, and inhibit left ventricular remodeling. (Deng, 2007)
Panax quinquefolium total saponins could decrease the left ventricular load, and decrease myocardial oxygen consumption, and increase the blood supply to the ischemic myocardium. (Liu et al 2001).
Polygonum multiflorum — Its ability to enhance myocardial anti-oxidant status under the conditions of ischemia reperfusion-induced oxidative stress has been proved (Yim et al, 2000).
Potassium – Hypokalemia increased the probability of ventricular tachycardia in patients with acute myocardial infarction. Thus, the follow up and treatment of hypokalemia in these patients is of special importance. (Pourmoghaddas et al 2012)
Potassium – Among inpatients with acute myocardial infarction , the lowest mortality was observed in those with postadmission serum potassium levels between 3.5 and <4.5 mEq/L compared with those who had higher or lower potassium levels. (Goyal et al 2012)
Resveratrol – Our results show that resveratrol improved left ventricle diastolic function, endothelial function, lowered LDL-cholesterol level and protected against unfavourable hemorheological changes measured in patients with coronary artery disease (CAD). (Magyar et al 2012)
Resveratrol – Previous studies have established that resveratrol can exert significant cardiovascular protective effects in various models of myocardial injury, hypertension, and type 2 diabetes. Recent studies provide clear evidence that resveratrol treatment can also confer vasoprotection in aged mice and rats, attenuating ROS production, improving endothelial function, inhibiting inflammatory processes and decreasing the rate of endothelial apoptosis. The mechanisms underlying the cardiovascular protective action of resveratrol are likely multifaceted. Resveratrol was shown to up-regulate eNOS and increase NO bioavailability. Resveratrol can also induce major cellular anti-oxidant enzymes (e.g. glutathione peroxidase, heme oxygenase, superoxide dismutase) in cardiac and vascular cells, which result in a marked attenuation of oxidative stress. Resveratrol both down-regulates vascular and cardiac expression of TNFα and inhibits NADPH oxidases in the vasculature. It is significant, that resveratrol was also shown to inhibit mitochondrial production of reactive oxygen species in the vasculature. In addition, resveratrol both in vivo and at nutritionally relevant concentrations in vitro was shown to inhibit inflammatory processes, including NF-κB activation, inflammatory gene expression and attenuation of monocyte adhesiveness to endothelial cells, all of which may contribute to its cardioprotective effects in aging. (Csiszar A 2011)
Rhodiola rosea extract – Our results suggest that the ethanol extract of Rhodiola has an ability to increase the cardiac output in STZ-diabetic rats showing heart failure. Also, an increase of PPAR-δ is responsible for this action of Rhodiola-ethanol extract. (Cheng et al 2012)
Rhodiola rosea extract – Pretreatment with extract of Rhodiola rosea decreased the incidence of ventricular fibrillation during ischemia in this animal study. (Arbuzov et al 2009)
Schisandrae chinensis – The protective effects of this agent were experimentally observed as to increase SOD activity of erythrocyte, markedly lowered the lipid hydroperoxide content of the venous blood, and lessen the myocardial infarct extent (Guo et al 2006)
Selenium – Dietary selenium intake influences post-infarct cardiac remodeling even when provided within the range of physiological values. Our data suggest that the cardioprotective effect of selenium might be mediated by a reduced oxidative stress, a lower connexin-43 dephosphorylation, and a decreased TNF-α expression. (Tanguy et al 2011)
Selenium – Glutathione peroxidase and the thioredoxin reductase are selenocysteine dependent enzyme systems, and their activity is known to be dependent upon an adequate supply of dietary selenium. Moreover, various studies suggest that the supply of selenium as a cofactor also regulates gene expression of these selenoproteins. As such, dietary selenium supplementation may provide a safe and convenient method for increasing antioxidant protection in aged individuals, particularly those at risk of ischemic heart disease, or in those undergoing clinical procedures involving transient periods of myocardial hypoxia. (Venardos et al 2007)
Vitamins C and E – The results suggest that early administration of antioxidant vitamins C and E in patients withacute myocardial infarction and concomitant diabetes mellitus reduces cardiac mortality. (Jaxa-Chamiec et al 2009)
Vitamins C and E – This randomized pilot trial shows that supplementation with antioxidant vitamins is safe and seems to positively influence the clinical outcome of patients with acute myocardial infarction. A larger study is warranted to provide further evidence of this promising and inexpensive regimen. (Jaxa-Chamiec et al 2005)
Vitamin D – Animal and human data indicate that vitamin D suppresses the activity of the renin-angiotensin system and improves endothelial function. Observational studies in humans suggest that low 25-hydroxyvitamin D (25[OH]D) levels are associated with a higher risk of hypertension. However, findings from randomized trials of vitamin D supplementation (with cholecalciferol or ergocalciferol) to lower blood pressure are inconsistent, possibly stemming from variability in study population, sample size, vitamin D dose, and duration. Supplementation with activated vitamin D (i.e., 1,25-dihydroxyvitamin D or analogues) in patients with chronic kidney disease reduces urine albumin excretion, an important biomarker for future decline in renal function. (Vaidya & Forman 2012)
Vitamin D is now recognized as important for cardiovascular health and its deficiency as a potential risk factor for several cardiovascular disease processes. (Vanga et al 2010)
Vitamin D – Data from prospective investigations suggest an inverse association between 25-OH-D andcardiovascular risk. However, given the heterogeneity and small number of longitudinal studies, more research is needed to corroborate a potential prognostic value of 25-OH-D for cardiovascular disease incidence and mortality. (Grandi et al 2010)
Vitamin D – The results of this study provide compelling evidence that a high vitamin D status is associated with improved survival in heart failure patients. (Liu et al 2010)
Vitamin E – Levels of oxidative-stress markers are increased, and concentrations of antioxidants (e.g., vitamin E) are decreased in patients with vasospastic angina. (Kusuma et al 2011)
Withania somnifera (Ashwagandha) – Post-ischemic reperfusion injury resulted in significant cardiac necrosis, apoptosis, decline in antioxidant status and elevation in lipid peroxidation in the IR control group as compared to sham. Withania somnifera prior-treatment favorably restored the myocardial oxidant-antioxidant balance, exerted marked anti-apoptotic effects {upregulated Bcl-2 protein, decreased Bax protein, and attenuated TUNEL positivity}, and reduced myocardial damage as evidenced by histopathologic evaluation. The antioxidant and anti-apoptotic properties of Withania somnifera may contribute to the cardioprotective effects. (Mohanty et al 2008)
Ziziphus – Total saponins of Semen Ziziphi spinosae are a kind of effective component extracted from Chinese medicine obtained from the seed of Ziziphus spinosa Hu. These agents have shown blood pressure lowering, anti-arrhythmic and anti-ischemic effects. (Yuan & Jing 2011)
Benefits of Exercise and Lifestyle Changes in Reducing the Risk of Heart Attacks or Heart Disease
Numerous clinical triggers of myocardial infarctions have been identified, including blizzards, the Christmas and New Year’s holidays, experiencing an earthquake, the threat of violence, job strain, Mondays for the working population, sexual activity, overeating, smoking cigarettes, smoking marijuana, using cocaine, and particulate air pollution. Avoiding clinical triggers or participating in therapies that prevent clinical triggers from precipitating cardiac events could potentially postpone clinical events by several years and improve cardiovascular morbidity and mortality. (Schwarz et al 2010)
Both coronary heart disease and ischaemic stroke share links to many of the same predisposing, potentially modifiable risk factors (hypertension, abnormal blood lipids and lipoproteins, cigarette smoking, physical inactivity, obesity and diabetes mellitus). This highlights the prominent role lifestyle plays in the origin of cardiovascular disease. (Lennon & Blake 2009)
Exercise regimens – The American College of Cardiology/American Heart Association recommends at least 30 minutes of moderate (at 50–70% of maximal predicted heart rate) exercise on most days to reduce the risk of cardiovascular events. Several human studies clearly demonstrate that chronic aerobic exercise regimens improve cardiovascular function. This is true not only in healthy subjects without any underlying risk factors, but also in older people, and those with cardiovascular risk factors. Indeed, those with cardiovascular risk factor/disease will benefit more. There is a much higher consistency in the results of studies which assess participants with cardiovascular disease/risk factors compared to healthy subjects. Patients with hypertension, type 2 diabetes, metabolic syndrome, stable cardiovascular disease, myocardial infarction, and congestive heart failure, all benefit from exercise training compared to those who do not participate in any training. Importantly, an exercise regimen that improves endothelial function in diabetic patients fails to benefit healthy subjects. In healthy individuals, a longer and more intense exercise protocol is needed to induce measureable changes in cardiovascular parameters, while older and sicker subjects can benefit from less intense exercise regimens. (Golbidi & Laher 2012)
Regular exercise reduces CRP, IL-6, and TNF-αlevels and also increases anti-inflammatory substances such as IL-4 and IL-10. In healthy young adults, a 12-week high-intensity aerobic training program down regulates cytokine release from monocytes. In fact, even leisure time physical activity (e.g., walking, jogging, or running, etc.) reduces hs-CRP concentration in a graded manner. Subjects with higher baseline CRP levels (>3.0mg/L) will benefit more. (Golbidi & Laher 2012)
Exercise training improved autonomic function, assessed by heart rate recovery, resting heart rate and systolic blood pressure, in the absence of changes in diet or medication. (Ribeiro et al 2012)
Exercise also resulted in an increase in mitochondrial antioxidant enzymes (copper-zinc superoxide dismutase, manganese superoxide dismutase, and glutathione peroxidase) and prevented the ischemia-reperfusion (IR)-induced release of proapoptotic proteins from the mitochondria. Collectively, these novel findings reveal that exercise-induced cardioprotection is mediated, at least in part, through mitochondrial adaptations resulting in a mitochondrial phenotype that resists IR-induced damage. (Lee et al 2012)
Exercise training has beneficial effects on left ventricular remodeling in clinically stable post-MI (myocardial infarction) patients with greatest benefits occurring when training starts earlier following MI (from one week) and lasts longer than 3 months according to this meta-analysis. (Haykowsky et al 2011)
Increased fitness. After adjusting for weight change, fitness was independently associated (p < 0.05) with improvements in R(2 )for glucose (+0.7%), HbA1c (+1.1%), high-density lipoprotein (HDL) cholesterol (+0.4%), and triglycerides (+0.2%) in ILI and diastolic BP (+0.3%), glucose (+0.3%), HbA1c (+0.4%), and triglycerides (+0.1%) in DSE. Taken together, weight and fitness changes explained from 0.1-9.3% of the variability in cardiovascular risk factor changes. Conclusion: Increased fitness explained statistically significant but small improvements in several cardiovascular risk factors beyond weight loss. (Gibbs et al 2012)
Stopping smoking, modifying one’s diet and exercise – This study found that individuals who change their behavior (quit smoking and modify diet and exercise) after acute coronary syndrome (ACS) are at substantially lower risk of repeat cardiovascular events. These benefits are seen early (<6 months), and the benefits from each behavior modification are additive. These results indicate that adherence to behavioral recommendations in the immediate postevent care of patients with ACS should be given as high a priority by physicians and caregivers as other secondary preventive medications and invasive strategies and justify a significant investment in establishing programs that systematically enhance early lifestyle modification and secondary prevention. (Chow et al 2010)
Transcendental Meditation – Randomized controlled trials, meta-analyses, and other controlled studies indicate this meditation technique reduces risk factors and can slow or reverse the progression of pathophysiological changes underlying cardiovascular disease. Studies with this technique have revealed reductions in blood pressure, carotid artery intima-media thickness, myocardial ischemia, left ventricular hypertrophy, mortality, and other relevant outcomes. The magnitudes of these effects compare favorably with those of conventional interventions for secondary prevention. (Walton et al 2002)
Reduce acute mental stress – Cardiovascular events can be triggered by acute mental stress caused by events such as an earthquake, a televised high-drama soccer game, job strain or the death of a loved one. Acute mental stress increases sympathetic output, impairs endothelial function and creates a hypercoagulable state. These changes have the potential to rupture vulnerable plaque and precipitate intraluminal thrombosis, resulting in myocardial infarction or sudden death. (Schwartz et al 2012)
Reduce chronic stress. Chronic stress has been shown to be associated with the development of cardiovascular disease and, in the case of particular types of stress such as job and marital strain, with recurrent adverse events afteracute myocardial infarction (AMI). (Arnold et al 2012)
Cholesterol, Statins and Heart Disease
Although reductions in all-cause mortality, composite endpoints and revascularisations were found with no excess of adverse events, there was evidence of selective reporting of outcomes, failure to report adverse events and inclusion of people with cardiovascular disease. Only limited evidence showed that primary prevention with statins may be cost effective and improve patient quality of life. Caution should be taken in prescribing statins for primary prevention among people at low cardiovascular risk. (Taylor et al 2011 Cochrane Database Syst. Rev.)
In view of the mounting evidence of a higher risk of diabetes with statins, specifically from the randomized trials — the FDA recently announced a label change to some statin therapies. Based on current evidence from the literature, a note of ‘an effect of statins on incident diabetes and increases in HbA1c and/or fasting plasma glucose’ has been added to the safety labelling of all drugs in the statin class. (Sattar & Taskinen 2012)
Herbal Remedies Supply a Novel Prospect for the Treatment of Atherosclerosis: A Review of Current Mechanism Studies – Increasing lines of evidence have questioned the statins-dominated treatment for atherosclerosis, including their dangerous side-effects such as the breakdown of muscle when taken in larger doses. Given the complicated nature of atherosclerosis and the holistic, combinational approach of herbal remedies, we propose that mixed herbal preparations with multiple active ingredients may be preferable for the prevention and treatment of atherosclerosis. (Zeng et al 2011)
Natural Compounds Which Can Be Used to Reduce the Dependency on Statins
Allicin – (which is formed when raw garlic is crushed, chopped or chewed) showed a favorable effect in reducing blood cholesterol, triglycerides, and glucose levels and caused a significant decrease in lowering the hepatic cholesterol storage. Accordingly, both in vivo and in vitro results demonstrated a potential value of allicin as a pronounced cholesterol-lowering candidate, providing protection against the onset ofatherosclerosis. (Lu et al 2012)
Anthocyanins – In this randomized controlled trial anthocyanin consumption significantly decreased the levels of serum high sensitivity C-reactive protein (hsCRP) (-21.6% vs. -2.5%, P = 0.001), soluble vascular cell adhesion molecule-1 (sVCAM-1) (-12.3% vs. 0.4%, P = 0.005) and plasma IL-1β (-12.8% vs. -1.3%, P = 0.019) compared to the placebo. We also found a significant difference in the LDL-cholesterol (-10.4% vs. 0.3%, P = 0.030) and HDL-cholesterol level changes (14.0% vs. -0.9%, P = 0.036) between the two groups. Anthocyanin mixture reduced the inflammatory response in hypercholesterolemic subjects. In addition, different anthocyanin compounds were found to have additive or synergistic effects in mediating anti-inflammatory responses in vitro cell culture assays. (Zhu et al 2012)
Artichoke leaf extract – Our results indicate that artichoke leaf extract may be useful for the prevention of hypercholesterolemia-induced pro-oxidant state in LDL+VLDL fraction and the reduction of increased serum cholesterol and triglyceride levels. (Kusku-Kiraz et al 2010)
Berberine, policosanol, red yeast rice, folic acid, CoQ10 and astaxanthin – In this study the authors have demonstrated that combined nutraceuticals (a pill containing berberine 500 mg, policosanol 10 mg, red yeast rice 200 mg, folic acid 0.2 mg, coenzyme Q10 2.0 mg, and astaxanthin 0.5 mg) significantly reduce cholesterolemia and achieved acceptable plasma LDL-C levels in elderly hypercholesterolemic patients who were previously statin-intolerant. Combined nutraceuticals are also safe and well tolerated in these patients. (Marazzi et al 2011)
Berberine, red yeast rice and policosanol – In this single centre, randomized, double-blind, placebo-controlled study on 50 hypercholesterolemic patients it was shown that this nutraceutical combination consisting of 500 mg berberine, 200mg red yeast rice and 10mg policosanol reduces cholesterol levels. The reduction is associated with improved endothelial function and insulin sensitivity. (Affuso et al 2010)
Curcumin – Long-term curcumin treatment lowers plasma and hepatic cholesterol and suppresses early atherosclerotic lesions comparable to the protective effects of lovastatin. The anti-atherogenic effect of curcumin is mediated via multiple mechanisms including altered lipid, cholesterol and immune gene expression. (Shin et al 2011)
DHA & EPA – The most compelling evidence for the cardiovascular benefit provided by omega-3 fatty acids comes from 3 large controlled trials of 32,000 participants randomized to receive omega-3 fatty acid supplements containing docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) or to act as controls.These trials showed reductions in cardiovascular events of 19% to 45%. These findings suggest that intake of omega-3 fatty acids, whether from dietary sources or fish oil supplements, should be increased, especially in those with or at risk for coronary artery disease. Patients should consume both DHA and EPA. (Lee et al 2008)
Epigallocatechin gallate (EGCG) – These results suggest that EGCG, a major component of green tea catechins, may decrease the risk of cardiovascular disease by reducing inflammatory markers in rats fed an atherogenic diet. (Ramesh et al 2010)
Flaxseed – Flax lignan complex (FLC), and secoisolariciresinol diglucoside (SDG), but not flaxseed oil,suppress atherosclerosis, and FLC and SDG slow progression of atherosclerosis but have no effect on regression. Flaxseed oil suppresses oxygen radical production by white blood cells, prolongs bleeding time, and in higher doses suppresses serum levels of inflammatory mediators and does not lower serum lipids. (Prasad K 2009)
Green tea extract – Considerable (P < .01) reductions in fasting serum glucose and insulin levels and insulin resistance were observed in the GTE group when compared with the placebo group. Serum tumor necrosis factor α and C-reactive protein were significantly lower, whereas total antioxidant status increased in the GTE group compared with the placebo (P < .05). Supplementation also contributed to significant (P < .05)decreases in the total and low-density lipoprotein cholesterol and triglycerides, but an increase in high-density lipoprotein cholesterol. In conclusion, daily supplementation with 379 mg of GTE favorably influences blood pressure, insulin resistance, inflammation and oxidative stress, and lipid profile in patients with obesity-related hypertension. (Bogdanski et al 2012)
Green tea extract – supplementation decreased several cardiovascular risk factors, including body composition, dyslipidemia, inflammatory status, and antioxidant capacity, in rats fed an atherogenic diet. This study supports green tea as an effective dietary component for sustaining cardiovascular health. (Bornhoeft et al 2012)
Guggulsterone – A recent study demonstrates that guggulsterone upregulates the bile salt export pump (BSEP), an efflux transporter responsible for removal of cholesterol metabolites, bile acids from the liver. Such upregulation of BSEP expression by guggulsterone favors cholesterol metabolism into bile acids, and thus represents another possible mechanism for its hypolipidemic activity. (Deng R 2007)
Lycopene – Our meta-analysis suggests that lycopene taken in doses ≥25mg daily is effective in reducing LDL cholesterol by about 10% which is comparable to the effect of low doses of statins in patient with slightly elevated cholesterol levels. More research is needed to confirm suggested beneficial effects on total serum cholesterol and systolic blood pressure. (Ried & Fakler 2011)
Niacin – The use of FDA-approved niacin (nicotinic acid or vitamin B3) formulations at therapeutic doses, alone or in combination with statins or other lipid therapies, is safe, improves multiple lipid parameters, and reduces atherosclerosis progression. Niacin is unique as the most potent available lipid therapy to increase high-density lipoprotein (HDL) cholesterol. (Villines et al 2011)
Oat β-glucan (a soluble dietary fiber that is found in the endosperm cell walls of oats) – Results of this analysis show that studies conducted during the past 13 years support the suggestion that intake of oat β-glucan at daily doses of at least 3 g may reduce plasma total and low-density lipoprotein (LDL)cholesterol levels by 5-10% in normocholesterolemic or hypercholesterolemic subjects. Studies described herein have shown that, on average, oat consumption is associated with 5% and 7% reductions in total and LDL cholesterol levels, respectively. Significant scientific agreement continues to support a relationship between oat β-glucan and blood cholesterol levels, with newer data being consistent with earlier conclusions made by the FDA and JHCI (United Kingdom Joint Health Claims Initiative). (Othman et al 2011)
Ocimum sanctum (Holy basil) – It can be concluded in this animal study that OS leaf extracts decreased hepatic and serum lipid profile, and provided the liver and cardiac tissues with protection from hypercholesterolemia. The lipid-lowering effect is probably due to the rise of bile acids synthesis using cholesterol as precursor, and antioxidative activity to protect liver from hypercholesterolemia.(Suanarunsawat et al 2011)
Olive leaf extract – In vitro, oleuropein and its major metabolite, hydroxytyrosol (which are polyphenols contained in olive leaf extract), exhibited a range of pharmacological properties beneficial for the cardiovascular system. These actions included enhanced nitric oxide production by mouse macrophages, antiinflammatory effects, protection against oxidative myocardial injury induced by ischemia and reperfusion , decreased blood pressure, inhibition of platelet aggregation and eicosanoid production, and scavenging of free radicals in addition to inhibition of 5- and 12-lipoxygenases . Oleuropein reduced infarct size, plasma lipid concentrations, and plasma markers of oxidative stress in cholesterol-fed rabbits. In vivo, olive leaf extract lowered blood cholesterol and lipid concentrations in cholesterol-fed rats and lowered blood pressure in nitro-L-arginine methyl ester-induced hypertensive rats as well as in normotensive rats. (Poudyal et al 2010)
Omega-3 polyunsaturated fatty acids – are found in fish oil and they have been shown to mitigate the risk of cardiovascular disease. They reduce fatal and nonfatal myocardial infarction, stroke, coronary artery disease, sudden cardiac death, and all-cause mortality. They also have beneficial effects in mortality reduction after a myocardial infarction. Omega-3 fatty acids have also been shown to have beneficial effects on arrhythmias, inflammation, and heart failure. They may also decrease platelet aggregation and induce vasodilation. Omega-3 fatty acids also reduce atherosclerotic plaque formation and stabilize plaques preventing plaque rupture leading to acute coronary syndrome. Moreover, omega-3 fatty acids may have antioxidant properties that improve endothelial function and may contribute to its antiatherosclerotic benefits. (Kar S 2011)
Policosanol, tomato extract, orally bioavailable grape procyanidins and Oenothera biennis (common evening primrose) oil – This randomized, double-blind, parallel-group trial showed that this rational combination of different compounds is effective and safe in lowering the elevated LDL-C and total cholesterol values. (Gupta et al 2012)
Red yeast rice (RYR) – Studies reviewed show that RYR significantly lowered LDL cholesterol and total cholesterol. Effects on triglycerides and HDL cholesterol were also observed in some studies. Compared with statins, RYR was shown to have an equal efficacy to statins when combined with or without other dietary supplements. RYR also appeared to be superior to placebo in preventing nonfatal myocardial infarction, total coronary heart disease events, and total deaths. (Yang & Mousa 2012)
Red yeast rice extract – The tested red yeast rice product demonstrated a significant cholesterol lowering effect compared to placebo, and was well tolerated in this Caucasian population. (Bogsrud et al 2010)
Red yeast rice extract – The treatment with a dietary supplement containing red yeast rice extract and policosanols has been for the first time successfully employed in hypercholesterolemic children. Results indicate this strategy as an effective, safe and well tolerated in a short-term trial. (Guardamagna et al 2011)
DHA & EPA – The most compelling evidence for the cardiovascular benefit provided by omega-3 fatty acids comes from 3 large controlled trials of 32,000 participants randomized to receive omega-3 fatty acid supplements containing docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) or to act as controls. These trials showed reductions in cardiovascular events of 19% to 45%. These findings suggest that intake of omega-3 fatty acids, whether from dietary sources or fish oil supplements, should be increased, especially in those with or at risk for coronary artery disease. Patients should consume both DHA and EPA. (Lee et al 2008)
Ginger (Zingiber officinale Roscoe), a well-known spice plant, has been used traditionally in a wide variety of ailments including hypertension. We report here the cardiovascular effects of ginger under controlled experimental conditions.These data indicate that the blood pressure-lowering effect of ginger is mediated through blockade of voltage-dependent calcium channels. (Ghayur & Gilani 2005)
Hawthorn (Crataegus oxyacantha) – Crataegus exerts mild blood pressure-lowering activity, which appears to be a result of a number of diverse pharmacological effects. It dilates coronary vessels, inhibits ACE, acts as an inotropic agent, and possesses mild diuretic activity. (Rewerski & Lewak 1967) (Uchida et al 1987) (Pepping et al 1995) (Weihmayr & Ernst 1996)
This study showed no herb–drug interactions arising from hawthorn administration. Taken concomitantly with prescribed medications, the herb demonstrated a hypotensive effect for patients with type 2 diabetes. (Walker et al 2006)
Olive leaf extract – In vitro, oleuropein and its major metabolite, hydroxytyrosol (which are polyphenols contained in olive leaf extract), exhibited a range of pharmacological properties beneficial for the cardiovascular system. These actions included enhanced nitric oxide production by mouse macrophages, antiinflammatory effects, protection against oxidative myocardial injury induced by ischemia and reperfusion, decreased blood pressure, inhibition of platelet aggregation and eicosanoid production, and scavenging of free radicals in addition to inhibition of 5- and 12-lipoxygenases . Oleuropein reduced infarct size, plasma lipid concentrations, and plasma markers of oxidative stress in cholesterol-fed rabbits. In vivo, olive leaf extract (OLE) lowered blood cholesterol and lipid concentrations in cholesterol-fed rats andlowered blood pressure in nitro-L-arginine methyl ester-induced hypertensive rats as well as in normotensive rats. (Poudyal et al 2010)
Omega-3 polyunsaturated fatty acids – are found in fish oil and they have been shown to mitigate the risk of cardiovascular disease. They reduce fatal and nonfatal myocardial infarction, stroke, coronary artery disease, sudden cardiac death, and all-cause mortality. They also have beneficial effects in mortality reduction after a myocardial infarction. Omega-3 fatty acids have also been shown to have beneficial effects on arrhythmias, inflammation, and heart failure. They may also decrease platelet aggregation and induce vasodilation. Omega-3 fatty acids also reduce atherosclerotic plaque formation and stabilize plaques preventing plaque rupture leading to acute coronary syndrome. Moreover, omega-3 fatty acids may have antioxidant properties that improve endothelial function and may contribute to its antiatherosclerotic benefits. (Kar S 2011)
Reserpine (which is in rauwolfia serpentina root) is effective in reducing systolic blood pressure roughly to the same degree as other first-line antihypertensive drugs. (Shamon & Perez 2009)
Andrographis – lowers blood pressure. It is a vasodilator. (Yoopan et al 2007)
Antioxidants – vitamin C (500 mg) vitamin E (200 iu), co-enzyme Q10 (60 mg) and selenium (100 mcg)caused significant increases in large arterial elasticity index (LAEI) as well as small arterial elasticity index (SAEI). A significant decline in HbA1C and a significant increase in HDL-cholesterol were also observed. This beneficial vascular effect was associated with an improvement in glucose and lipid metabolism as well as decrease in blood pressure. (Shargorodsky et al 2010)
Antioxidants – A significant body of epidemiological and clinical trial data suggest that diets known to contain significant concentrations of naturally occurring antioxidants appear to reduce blood pressure and may reduce cardiovascular risk. Data suggest, regardless of etiology, excessive ROS is a common factor in the pathogenesis and morbidity of hypertension.(Kizhakekuttu & Widlansky 2010) Foods rich in antioxidants include cranberries, blueberries, raspberries, blackberries, beans, artichokes, Russet potatoes, walnuts and hazelnuts. (Wu et al 2004)
Antioxidants copper, manganese, and zinc – The mean arterial blood pressure showed significant positive correlation with glucose, total cholesterol, triglyceride, low-density lipoprotein cholesterol, very low-density lipoprotein cholesterol, atherogenic index, insulin resistance and malondialdehyde while high density lipoprotein-cholesterol and total antioxidant activities showed negative correlation. The result therefore indicated strong relationship between oxidative stress and hypertension and underscores the role of antioxidant minerals in reducing oxidative stress, dyslipidemia, and insulin resistance associated with hypertension. (Muhammad et al 2012)
Beetroot juice – lowers blood pressure. Only 250 ml is necessary to have this effect. (Kapil et al 2010)
Capsaicin (in chili peppers) – can improve blood vessel function and lower blood pressure. (Yang et al 2010)
Carrots – Daucus carota (carrot) has been used in traditional medicine to treat hypertension. Activity-directed fractionation of aerial parts of D. carota resulted in the isolation of two cumarin glycosides coded as DC-2 and DC-3. These results indicate that DC-2 and DC-3 may be acting through blockade of calcium channels and this effect may be responsible for the blood pressure lowering effect of the compounds observed in the in vivo studies. (Gilani et al 2000)
Coenzyme Q10 – lowers blood pressure. (Burke et al 2001) (Singh et al 1999) A number of trials provide clinical evidence that some patients with high blood pressure may benefit from coenzyme Q10 supplementation. (Wyman 2010) Early data from non-controlled studies in human hypertension demonstrate reductions in blood pressure with CoQ supplementation. Further, small randomized studies using a CoQ dose of 100–120mg daily have demonstrated significant reductions in blood pressure with minimal side effects in patient with Stage II hypertension. Interestingly, a new, mitochondrial-targeted formulation of CoQ has demonstrated anti-hypertensive efficacy in a rat model. (Kizhakekuttu & Widlansky 2010)
Coleus forskohlii – Its predominant effect is to lower the blood pressure of anaesthetised cat and rat as well as of the spontaneously hypertensive rat due to relaxation of the vascular smooth muscle. In small doses it has a positive inotropic effect on isolated rabbit heart as well as on cat heart in vivo. (Dubey et al 1981)
Egg white peptides – exhibited antihypertensive activity in vivo. (Garcia-Redondo et al 2010)
Garlic – has been shown to reduce systolic blood pressure by 5.5% in animal studies. (Tapsell et al 2006) These findings point out the beneficial effects of garlic supplementation in reducing blood pressure and counteracting oxidative stress in humans, and thereby, offering cardioprotection in essential hypertensives. (Dhawan & Jain 2005) The effect of garlic on blood pressure cannot be ascertained. Previous meta-analyses have been based on trials with inadequate study designs, methodological deficiencies and with too little information about blood pressure measurement. In our view, use of garlic cannot be recommended as antihypertensive advice for hypertensive patients in daily practice. (Simons et al 2009) Our meta-analysis suggests that garlic preparations are superior to placebo in reducing blood pressure in individuals with hypertension. (Ried et al 2008)
Green or Oolong tea – Habitual moderate strength green or oolong tea consumption, 120 mL/d or more for 1 year, significantly reduces the risk of developing hypertension in the Chinese population. (Yang et al 2004)
Magnesium – intake of 500 mg/d to 1000 mg/d may reduce blood pressure (BP) as much as 5.6/2.8 mm Hg. However, clinical studies have a wide range of BP reduction, with some showing no change in BP. The combination of increased intake of magnesium and potassium coupled with reduced sodium intake is more effective in reducing BP than single mineral intake and is often as effective as one antihypertensive drug in treating hypertension. Reducing intracellular sodium and calcium while increasing intracellular magnesium and potassium improves BP response. Oral magnesium acts as a natural calcium channel blocker, increases nitric oxide, improves endothelial dysfunction, and induces direct and indirect vasodilation. (Houston 2011) Our meta-analysis detected dose-dependent BP reductions from magnesium supplementation. (Jee et al 2002)
Oats – The addition of oat cereals to the normal diet of patients with hypertension significantly reduces both systolic blood pressure and diastolic blood pressure. Soluble fiber-rich whole oats may be an effective dietary therapy in the prevention and adjunct treatment of hypertension. (Keenan et al 2002)
Resveratrol – improved hypertension, dyslipidemia, hyperinsulinemia in vivo. (Rivera et al 2009)
Royal Jelly peptides – were effective in lowering blood pressure in vivo. (Tokunaga et al 2004)
Salmon – Salmon consumption three times per week can decrease diastolic blood pressure (DBP) similar to fish oil and significantly more than lean fish during an 8-wk energy restriction in young overweight individuals. A lower DHA content in erythrocyte membrane at baseline, which might identify infrequent fish eaters, is associated with a greater DBP reduction in the course of an 8-wk dietary intervention providing fatty seafood. (Ramel et al 2010)
Sesame – These findings suggest that sesamin (a lignan from sesame oil) feeding inhibits enhanced vascular O2- production in DOCA-salt hypertensive rats and that the antioxidative action of sesamin may contribute to its antihypertensive activity. (Nakano et al 2002)
Watermelon – can be an effective natural weapon against pre-hypertension. When 6 gms of the amino acidL-citrulline/L-arginine from watermelon extract was administered daily for 6 weeks there was improved arterial function and consequently lowered aortic blood pressure in all nine of the pre-hypertensive subjects. (Figueroa et al 2010)
Vitamin D deficiency is an independent risk factor for hypertension. Epidemiological and clinical studies have long shown an association between inadequate exposure to sunlight, vitamin D deficiency and hypertension or increased plasma-renin activity. This is additionally underlined by the fact that mean blood pressure values are lower in summer than in winter. Persons with vitamin D insufficiency [25(OH)D < 30 ng/ml] have a 3.2-fold higher risk of developing hypertension than persons with a good vitamin D status. A recently published systematic review and meta-analysis came to the conclusion that vitamin D produces a fall in systolic blood pressure of −6.18 mmHg and a nonsignificant fall in diastolic blood pressure of −2.56 mmHg in hypertensive patients. (Grober & Kisters 2012)
Animal studies have shown that vitamin D deficiency increases blood pressure through an interaction with the renin-angiotensin system. In genetically altered mice (so-called vitamin D receptor null mice), which cannot synthesize vitamin D, it was observed that renin expression, the activity of the renin-angiotensin system, and the production of angiotensin II were drastically increased. The mice developed hypertension, cardiac hypertrophy, and edema. These observations correlate with those made in normal mice, in which inhibition of vitamin D biosynthesis led to a rise in renin expression, whereas the injection of 1,25(OH)2D suppressed renin expression. (Grober & Kisters 2012)
Other mechanisms contributing to the antihypertensive effect of vitamin D are the direct effects of 1,25(OH)2D on endothelial function, parathyroid hormone secretion and insulin sensitivity. Vitamin D and magnesium have a mutually enhancing effect on endothelial function and vascular reactivity and on many metabolic processes (e.g., insulin metabolism). The antihypertensive effect of magnesium has been demonstrated in numerous interventional studies. Although administration of vitamin D and magnesium alone to patients with hypertension (severity II or III) is not likely to normalize blood pressure according to the WHO criteria, supplementation of vitamin D and magnesium monitored by laboratory-diagnostic tests may nevertheless allow attempts to reduce the dosage of other antihypertensive substances (e.g., diuretics and ACE inhibitors). This could certainly reduce many side effects of the antihypertensive drugs used (e.g., disturbances of glucose tolerance). (Grober & Kisters 2012)
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