FIELD OF INVENTION The present invention relates to a mouth diss.olving (through oral delivery system) nutraceuticaJ tablet and method for preparing the same. More particularly the present invention relates to a mou~:1 dissolving nutraceutical tablet and method for preparing mouth dissolving nutraceutical tablet from the extract of Beet root and hawthorn berry herbs with Sodium nitrite, Ascorbic acid, Mecobalamin and L Citrulline. Nutraceutical tablet is meant to increase or Restore Nitric oxide level in the body. This is natural way to increase nitric oxide in the body. Nitric oxide is an impurlant signaling molecule, which is required for healthy blood circulation. BACKGROUND OF THE INVENTION The mammalian biosynthesis of nitric oxide (NO) discovered in the 1980's for its roles in the immune, cardiovascular and nervous systems established ~ startling new paradigm in the hislury of cellular signaling mechanisms. Nitric oxide is a gas that occurs naturally throughout the body. NO is a powerful signaling molecule that causes the walls of blood vessels to relax, improving circulation. Its production by vascular endothelium is particularly important in the regulation C'f blood flow. Any decrease in NO production or Joss in generation of NO due to dysfunctional vascular endothelium is a very likely cause of heart disease. Experimental and clinical studies also demonstrate that insufficient nitric oxide production is associated with major cardiovascular risk factors, such as hyperlipidemia, diabetes, hypertension, smoking and atherosclerosis. Unfortunately, the ability to generate nitric oxide decreases with age resulting in increased risk of heart and vascular disease. Prior to this discovery, NO was widely recognized as a toxic molecule: a common air pollutant, a constituent of cigarette smoke, and a toxic gas, which ap!'lears in the exhaust of motor cars and jet airplanes, causes acid rain, and destroys the ozone layer. Thus, it was essentially inconceivable that cells would intentionally produce a toxic gas as part of normal physiology. Referring to Figure 1, NO is now recognized as one of the most important signaling molecules in the body, and is involved in virtually every organ system where it is responsible for modulating an astonishing variety of effects. The primary targets for NO are metals and thiols. NO can bind to soluble gualylylcyclase (sGC) and cause an increase in second messenger cGMP, and mediate a number of physiological functions. This pathway was considered the basis of NO based signaling until it was recognized that NO elicited a number of physiological and biological effects that were not dependent upon cGMP. It is now recognized that NO can react directly with thiyl radicals to form nitrosothiols or other reaction products of NO i.e., nitrite, N20 3, N20 4, which can post-translationally modify thiols to affect protein structure and function. NO has been shown to be involved in and affect practically every organ system in the body. One can then imagine a host of diseases or conditions and multi-systemic symptoms may be caused or affected by the body's dysregulation of NO production/signaling (referring to Figure 1). Maintaining NO homeostasis is critical for optimal health and disease prevention. Developing novel NO based diagnostics and therapies is central to better patient care, especially in the geriatric patient. The first pathway to be discovered for the endogenous production of NO was involving Larginine, from a group of enzymes call nitric oxide synthase (NOS). NOS enzymes produce NO by catalyzing a five electron oxidation of the guanidino nitrogen uf L-arginine. Oxidation of Larginine to L-citrulline occurs via two successive mono-oxygenation reactions producing NOhydroxy- L-arginine as an intermediate. Two moles of 0 2 and 1.5 moles of nicotinamide adenine dinucleotide phosphate (NADPH) are consumed per mole of NO formed. NOS enzymes are the 2 ------------------ only enzymes known to simultaneously require multiple bound cofactors/prosthetic groups: flavin adenine dinucleotide (FA D), flavin mononucleotide (FMN), heme, glutathione, NADPH, tetrahydrobiopterin (Blit) and Ca2+ ~calmodulin. There are three isoforms of NOS, the genetic se~uence of each residing on three distinct chromosomes. One type is constitutive, Ca +/calmodulin dependent and releases NO for short time periods in response to receptor or physical stimulation. NO released by this enzyme acts as a transduction mechanism underlying several physiological responses. The other enzyme type is induced after activation of macrophages, endothelial cells and a number of other cells by cytokines and once expressed, synthesizes NO for long periods of time. Furthermore, this enzyme is Ca2+ independt::nt since calmodulin is already bound to the enzyme, and its induction is inhibited by glucocorticoids. Endothdial NOS (eNOS), neuronal NOS (nNOS) which are both constitutively expressed in mammalian cells have now been well characterized in the cardiovasc.nll'lr· system and nervous ~>ystom rcspcctively, and an inducible NOS(iNOS) which was first believed to be expressed only when activated by an immune response. Now it is appreciated that eNOS is found in other cells and tissues besides the endothelium, iNOS is found constitutively in some tissues, and there are inducible forms of both eNOS and nNOS; adding confusion to the nomenclature as it was first described. In an attempt to clarify the nomenclature, the three different isoforms are now commonly referred to as NOSI, NOSH, and NOSIII for neuronal, inducible and endothelial isoforms, respectively, based on the order in which they were first purified and cloned. For years, scientists and physicians have investigated L-arginine supplementation as a means to enhance NO production. This strategy has been shown to work effectively in young healthy individuals with functional endothelium or in older patients with high levels of asymmetric dimethyl. L-arginine (ADMA) where the supplemental L-arginine could outcompete this natural inhibitor of NO production. Patients with endothelial dysfunction, however, by definition, are unable to convert L-arginine to NO and, therefore, this strategy has failed in clinical trials. Schulman et a!. found that L-arginine, when added to standard post infarction therapies, did not improve vascular stiffness measurements or ejection fraction and was associated with higher post infarction mortality. L-arginine should not be recommended following acute myocardial infarction (MI). However, there are also a number of studies showing benefit to patients taking L-arginine just as many showing no benefit, no harm. Understanding the complex and complicated reaction pathway for NOS mediated production of NO from L-arginine helps us define the context for rational interventions. Using L-arginine supplementation therapy alone may not be effective due to oxidative stress in geriatric patients resulting in constitutive NOS uncoupling by redox-based post translational modifications. Supplementing L-arginine with anti-oxidants to prevent oxidation of reduced co-factors such as BH4, might prevent NOS uncoupling and lead to better results. In a study by Taddei et a!., the role of oxidative stress on NO availability and endoth.elial dysfunction was examined in both younger and older aged populations. They found that NO availability was profoundly restored in older patients when oxidative stress is removed by antioxidants such as vitamin C. In older individuals (age> 60 years) characterized by a profound alteration in NO availability, vitamin C not only enhanced the response to the endothelial agonist but also restored the inhibitory effect of L-NMMA on vasodilation to acetylcholine. Although, it is demonstrated that anti-oxidant supplementation can be very beneficial for those experiencing oxidative stress and endothelial dysfunction, it showed no benefit in younger (age < 60) or healthy individuals with no 3 ,r,' '' ' ' endothelial dysfunction. Collectively, the literature suggests that strategies to enhance NO production through L-arginine supple mentation are equivocal at best. Although the L-arginine-NO pathway was the first to be discovered, it does not necessarily mean it is the primary pathway for the endogenous production of NO. In fact nitrogen cycling in bacteria and production of NO as an intermediate in denitrification may be one of the most primitive pathways known, dating back to the Archaean era. The now recognized human nitratenitrite- nitric oxide pathway that still relies on bacteria may be a redundant system for overcoming the body's inability to make NO from L-arginine. It appears that we have at least two systems for affecting NO production/homeostasis. The first is through the classical L-arginlneNO pathway. This is a complex and complicated five-electron oxidation of L-arginine and if any of the co-factors become limiting, then NO production from NOS shuts down, and iu many cases, NOS produces superoxide instead. The enzymatic production of NO normally proceeds very efficiently. However, in disease characterized by oxidative stress where essential NOS co factors become oxidized, NOS uncoupling, or conditions of hypoxia where oxygen is limiting, this process can no longer maintain NO production. This process is illustrated in Figure 2. Therefore, one can argue saliently that there has to be an alternate route for NO production. It is highly unlikely that nature devised such a sophisticated mechanism of NO production as a sole source of a critical molecule. This alternate route involves the provision of nitrate and nitrite reductively recycled to NO (Figure 3). The two-electron reduction of nitrate to nitrite occurs through symbiosis with facultative anaerobic bacteria that reside in the crypts of our tongue. Nitrite reduction to NO can occur in a much simpler mechanism than nitrate. The 1-electron reduction of nitrite can occur by ferrous heme proteins (or any redox active metal) through the following reaction: N02 - + Fe(II) + H+ ~NO+ Fe(III) + Oir This ·is the same biologically active NO as that produced by NOS, with nitrite rather than Larginine as the precursor and is a relatively inefficient process. Much of the recent focus on nitrite physiology is due to its ability to be reduced to NO during ischemic or hypoxic events. Nitrite reductase activity in mammalian tissues has been linked to the mitochondrial electron transport system, protonation, deoxyhemoglobin, and xanthine oxidase.. Therefore, for this reaction to occur, the tissues or biological compartment must have a sufficient pool of nitrite stored. Since plasma nitrite is a direct measure of NOS activity, a compromised NOS system can also affect downstream nitrite production and metabolism, which can perhaps exacerbate any condition associated with decreased NO bioavailability. Considerable published data support the notion that exogenous nitrite contributes to whole body NO production: NO produced from nitrite in the upper intestine is up to 10,000 times the concentrations that occur in tissues from enzymatic synthesis, nitrite can act as a circulating NO donor, and nitrite can itself perform many aCtions previously attributable to NO without the intermediacy of NO. Experiments in primates revealed a beneficial effect of long-term application of nitrite on cerebral vasospasm. Moreover, inhalation of nitrite selectively dilates the pulmonary circulation under hypoxic conditions in vivo in sheep.Topical application of nitrite improves skin infections and ulcerations. Replenishing nitrate and nitrite through dietary means may then act as a protective measure to compensate for insufficient NOS activity under conditions of hypoxia or in a number of conditions characterized by NO insufficiency. Since a substantial portion of steady state nitrite concentrations in blood and tissue are derived from dietary sources, modulation of nitrite and/or nitrate intake may provide a first line of defense for conditions associated with NO insufficiency. 4 The recognition of this mammalian nitrogen cycle has led researchers to explore the role of dietary nitrate and nitrite in physiological processes that are known to be regulated by NO. Nitrite can transiently form nitrosothiols (RSNOs) under both normoxic and hypoxic conditions and a recent study by Bryan et al. demonstrates that steady state concentrations of tissue nitrite and nitroso are affected by changes in dietary nitrite and nitrate (collectively, NOx) intake. Furthermore, enriching dietary intake of nitrite and nitrate translates into significantly less injury from heart attack. Previous studies demonstr"-ted that nitrite therapy given intravenously prior to reperfusion protects against hepatic and myocardial ischemia/reperfusion (1/R) injury. Additionally, oral nitrite has also been shown to reverse L-NAME induced hypertension and serve as an alternate source of NO in vivo. These results have since been corroborated in humans. ·In fact, it has been reported that dietary nitrate reduces blood pressure in healthy volunteers. Commercial development of nitrite and nitrate enriched dietary supplements has been shown to impact important cardiovascular risk factors in the aging population leading to a reduction in triglycerides and restoration of NO homeostasis. Furthermore, in the stomach, nitrite-derived NO seems to play an important role in host defense and in. regulation of gastric mucosal integrity. However, this is pH dependent. Since stomach acid production declines with age and many patients are prescribed proton pump inhibitors, this pathway may be disrupted in the geriatric patient causing additional problems with maintaining NO homeostasis. Nitrite and nitrate therapy may then offer an all natural, over the counter and cost effective regimen for conditions associated with NO insufficiency. This has the potential to provide the basis for new preventive or therapeutic strategies and new dietary guidelines for optimal health. From a public health perspective, we may be able to make better recommendations on diet and dramatically affect the incidence and severity of cardiovascular disease and the subsequent clinical events. The major pathway for NO metabolism is the stepwise oxidation to nitrite and nitrate. For years, both nitrite (N02 -) and nitrate (N03 ) have been used as surrogate markers of NO production in biological tissues, but there have not been any new developments in the use ofNO biomarkers in · t;te c:inical setting for diagnostic or prognostic utility. In fact, NO status is still not part of the standard blood chemistry routinely used for diagnostic purposes. This is simply unacceptable given the critical nature of NO in many disease processes and new technologies should be developed. The only true measure of endothelial NO production (endothelial function) is through flow mediated dilatation (FMD). FMD is a non-invasive ultrasound-based method where arterial diameter is measured in response to an increase in shear stress, which causes release ofNO from the endothelium and consequent endothelium dependent dilatation. FMD has been shown to correlate with invasive measures of endothelial function, as well as with the presence and severity of the major traditional vascular risk factors. Nitrite and nitrate have recently been shown ~o be biomarkers for cardiovascular and other diseases from both diagnostic and therapeutic aspects. However, it is not known if levels of NOx correlate with FMD. In addition to blood, urinary levels of NOx provide a means to assess systemic NO production in vivo, or renal: handling of these anions which may be compromised in the geriatric patient. A report by Kleinbongard et al. demonstrated that plasma nitrite levels in humans progressively decrease . with increasing cardiovascular risk load. Risk factors included age, hypertension, smoking, and hypercholesterolemia, conditions all known to reduce the bioavailability of NO. Although a correlation exists in the plasma, it is not known whether the situation is mirrored in the heart or other tissue of interest in specific disease. The recent recognition of a .human nitrogen cycle 5 whereby nitrate .and nitrite are reduced to NO by an enterosalivary circulation of nitrate now opens up the potential for using saliva as a potential· biomarker for NO status in certain diseases. Aging and hypertension are well-documented cardio vascular risk factors. Most of the functional and structural vascular alterations that lead to cardiovascular complications are similar in aging and hypertension. Moreover, these vascular changes associated with essential hypertension are generally considered to be an accelerated form of the changes seen with aging. When we are young and healthy, the endothelial production of NO through L-arginine is efficient and sufficient; however, as we age we lose our ability to synthesize endothelial derived NO. Most of the works on the activity of NO in cells and tissues agree that the bioavailnbility or the gem:ration of NOS derived NO decreases with aging. It has been proposed that superoxide can scavenge NO to form peroxynitrite and thereby reduce its effective concentrations in cells. It has also bt:t:n reported that there is decreased NOS expression with aging both in constitutive and inducible isoforms. Berkowitz etal.observed the upregulation of arginase (an enzyme that degrades the natural substrate for NOS, L-arginine) in aged blood vessels and the corresponding modulation of NOS activity. Taddei et al. have shown that there is a gradual decline in endothelial function due to aging with greater than 50% loss in endothelial function in the oldest age group tested as measured by forearm blood flow assays. Egashiraet al. reported more dramatic findings in the coronary circulation of aging adults whereby there was a loss of 75% of endothelium-derived nitric oxide in 70-80 year old patients compared to young, healthy 20 year olds. Vita et aL demonstrated that increasing age was one predictor of abnormal endotheliumdependent vasodilation in atherosclerotic human epicardial coronary arteries. Gerhard et al. conclUded from their 1996 study that age was the most significant predictor of endotheliumdependent vasodilator responses by multiple stepwise regression analysis. Collectively, these important findings illustrate that endothelium-dependent vasodilation in resistance vessels declines progressively with increasing age. This is illustrated in Figure 4. This abnormality is present in healthy adults who have no other cardiovascular risk factors, such as diabetes, hypertension, or hypercholesterolemia. Most of these studies found that impairment of endothelium-dependent vasodilation was clearly evident by the fourth decade. In contrast, endothelium-independent vasodilation does not change significantly with aging, demonstrating that the responsiveness to NO does not change only the ability to generate it. These observations enable us to conclude that reduced availability of endothelium-derived NO occurs as we age, and to speculate that this abnormality may create an environment that is conducive to atherogenesis and other vascular disorders, including Alzheimers disease. It appears that aging interrupts NO signaling at every conceivable level, from production to inactivation. Given that NO is a necessary molecule for maintenance of health and prevention of disease,· restoration of NO homeostasis may provide a new treatment modality for age and age related disease. Aging is considered the single largest risk factor related to cardiovascular related diseases and deaths. Cardia-protection decreases with increasing age and is attributed to a decline in NO. The lack of NO production can lead to hypertension, atherosclerosis, peripheral artery disease, heart failure, and thrombosis leading to heart attack and stroke, especially in geriatrics. Remarkably, all of these conditions have been shown to be positively affected by dietary nitrite and nitrate interventions. Hypertension, along with aging is a well-known cardiovascular risk factor that leads to functional and structural alterations in the heart and vasculature. Vascular changes associated 6 with hypertension, such as endothelial dysfunction, are an accelerated form of the type of changes seen with aging. Additionally, the prest:nce of acetyl choline alongside a NO synthase inhibitor (L-NMMA) was tested for NO availability in the vasculature. A noteworthy finding is that after the age of 60 years old, the inhibiting effect of L-NMMA on response to acetylcholine was extremely weak, suggesting that NO availability is completely compromised in older populations. These results indicate that essential hypertension is characterized by an age-related reduction of endothelial function by mechanisms that appear to be similar to those observed in olut:r normotensive 'individuals. NO based therapies can reduce blood pressure. Transdermal nitroglycerin has been shown to reduce blood pressure in patients with recent stroke. Dietary intervention with nitrite and nitrate has been shown to modestly reduce blood pressure in humans showing remarkable efficacy using this approach. Atherosclerosis is the major source of morbidity and mortality in the developed world. The magnitude of this problem is profound, as atherosclerosis claims more lives than all types of cancer combined and the economic costs are considerable. Reduced NO availability is a hallmark of atherosclerosis. The endothelium-derived NO plays a crucial role in regulating a wide spectrum of functions in the cardiovascular system, including vasorelaxation, · inhibition of leukocyte-endothelial adhesion, vascular smooth muscle cell (SMC) migration and proliferation, as well as platelet aggregation. Th~ concept of endothelial dysfunction arises from variations in blood flow observed in patients with atherosclerosis compared with healthy subjects. In healthy subjects, activation of eNOS causes vasodilation in both muscular conduit vessels and resistance arterioles. In contrast, in subjects with atherosclerosis, similar stimulation yields attenuated vasodilation in peripheral vessels and causes paradoxical vasoconstriction in coronary arteries, thus indicating a decrease in the production and/or bioavailability of NO. Interestingly, endothelial dysfunction can be demonstrated in patients with risk factors for atherosclerosis in the absence of atherosclerosis itself. These observations lend credence to the concept that endothelial dysfunction is integral to the development and progression of disease. Impaired endo~helium may abnormally reduce vascular perfusion, produce factors that decrease plaque stability, and augment the thrombotic response to plaque rupture. There are a number of studies showing that insufficient NO production from the eqdothelium is associated with all major cardiovascular risk factors, such as hyperlipidemia, diabetes, hypertension, smoking and severity of atherosclerosis, and importantly also has a profound predictive value for the future atherosclerotic disease progression. Augmentation ofNO or restoration of NOS function seems a logical means to inhibit atherosclerosis. Absence of eNOS in apoE-knockout mice accelerates atherosclerosis that is not caused by hypertension. Paradoxically, however, overexpression of endothelial NOS accelerates lesion formation in apoE-deficient mice demonstrating that enhanced NOS derived NO may not always be beneficial. Supplementation with tetrahydrobiopterin (BH4) reduced the lesion size to those seen in Apo. E knockout mice revealing the requirement of enzyme cofactors. Even with BH4 supplementation there was still no effect on lesion . development. These ·studies demonstrate . the complexity of endothelium derived NO in the setting of atherosclerosis but clearly illustrate the dysfunctional eNOS/NO pathway as an early marker or a common mechanism for various cardiovascular disorders and therefore provides an ideal target for therapeutic or preventive intervention including alternative NOS independent sources of NO. Stokes et a!. have demonstrated that supplementing nitrite in the drinking water inhibits the adhesion · and emigration of leukocytes to the vascular endothelium, one of the earliest events of atherogenesis suggesting this nitrate-nitrite-NO pathway may be useful in preventing chronic vascular disease. 7 _).,. I Thrombosis affects nearly 1 million patients in the United States annually. Out ofthose million, nearly 300,000 are reported as thrombosis related deaths. A majority of current treatment options are centered on preventative anticoagulants, such as warfarin but with risk of bleeding. NO inhibits platelet activation, adhesion, and aggregation by influencing several signaling pathways, including activation of sGC . and increasing intracellular cGMP; inhibition of phosphatidylinositol-3 kinase; and inhibition of capacitativecation influx and agonist-dependent increases in intracellular calcium. These molecular events lead to an impairment of platelet a.ctivatiun, adhesion, secretion, fibrinogen-binding to glycoprotein lib/Ilia, and ultimately, aggregation. In addition, NO promotes platelet disaggregation. In conjunction with its vasorelaxing actions, these anti-platelet effects of NO ml;lintain blood fluidity and tissue perfusion. A constitutive NO synthase has been found in both human platelets and megakaryocytic cells and this isoform is active. Using an NO-selec.tive microelec.trodc adapted to a platelet aggregometer, Freedman et al. recently showed that this platelet-derived NO not only modestly modulates platelet activation to strong and weak agonists but, more importantly, markedly inhibits platelet recruitment to the growing platelet thrombus. NO, derived both from the endothelial cell and the platelet, modulates platelet activation, adhesion, and aggregate formation, thereby serving as an important deterrent to platelet-mediated arterial thrombosis. NO insufficiency, either through reduced production or oxidative inactivation leads to thrombotic events.Efforts to restore the normal vascular redox balance and/or to restore normal NO availability may provide one therapeutic avenue for reducing platelet-dependent arterial thrombosis in older patients. In fact, recent studies have shown that dietary nitrate can inhibit platelet aggregation again demonstrating this dietary approach to replete NO may provide first line of defense for NO insufficiency. The most feared disease of the geriatric population is Alzheimer's disease (AD). In the United States, around 5.4 million people live with AD, a type of dementia. Patients with AD lose brain function, resulting in problems with language, perception and memory. AD can start before age 60 (early onset) or after age 60 (late onset). The risk for AD increases as a person ages and that rising risk is being seen as the baby boomers start turning 65 years old. Out of every eight baby boomers, one will get AD after she turns 65 years old; at age 85, that risk grows to one in two. With the 65 and over population in the United States expected to double by 2030, there may be up to 16 million people with AD by 2050; there may be almost one million new AD cases diagn~sed each year. Each year in the United States, inore than 800,000 people die from this neurological disease~ It is the sixth leading cause of death, with the number of deaths rising 66 percent from 2000 to 2008. There is becoming a clear and convincing association with AD and NO. Decreased levels of NOx has been detected in patients with different forms of dementia especially AD. The exact etiology of sporadic AD is unclear, but it is interesting that cardiovascular risk factors including hypertension, hypercholesterolemia, diabetes mellitus, aging, and sedentary lifestyle. are associated with higher incidence of AD. The link between cardiovascular risk factors and AD has yet to be identified; however, a common feature is endothelial dysfunction, specifically, decreased bioavailability of NO. The pathogenesis of Alzheimer's disease is closely associated with the accumulation of amyloid-~ (A~) peptides, which eventually form neuronal deposits known as senile plaques on the outside surface of the neurons and lead to neuron death. AD is characterized by progressive loss of neurons, cognitive decline, and two defining histopathologies: extracellular amyloid plaques and intracellular tangles composed primarily of 8 A~ peptide and hyperphosphorylated tau, respectively. Furthermore, AD is often accompanied by cerebrovascular dysfunction, as well as amyloid deposition within the cerebral vessels, termed cerebral amyloid angiopathy. NO in the brain can be produced either by iNOS in microglia and astrocytes, or by constitutive NOS in neurons and endothelial cells (nNOS and eNOS). A large body of evidence suggests that the NO produced by neuronal and endothelial constitutive NOS is responsible for neuroprotection during A~-induced cell death, while NO production in the case of iN OS activation plays a neurotoxic role due to the inflammatory response caused by the over generation of other reactive nitrogen species from NO.A decrease in nNOS and an increase in hippocampal iNOS have been demons trated in aged rats, suggesting the dual roles and complexity of NO signaling in the brain and durine AD. In mice; higher levels of constitutivt! NO produced by NOS protects beta-amyloid transgenic mice from developing most typical human symptoms of AD.The protective role of NO in AD pathogenesis has been linked to NO/sf.jC/cGMP/Protein Kinase G (PKG) signaling cascades. Treatment with NO donors and cGMP analogues suppresses cell death, and increasing intracellular cGMP levels prevents inflammatory responses in brain cells. Moreover, the use ofthe NO donors, sGC stimulators, and cGMP-analogs reverses learning and memory impairment through PKG activation, in part by reestablishing the enhancement of the transcription factor cAMP-responsive element binding protein (CREB), which is phosphorylated during long term potentiation. It has also been shown that NO modulates expression and processing of amyloid beta precursor protein. However, an accumulation of A~ inhibits the NO signaling pathway and therefore may suppress the protective effects of endogenous NO in the brain. Chronic administration of fibrillar AP decreases the expression of sGC in cultured rat astrocytes, desensitizing them to treatment with sodium nitroprusside. Acute A~ administration blocks NO-induced vasoactivity in rats [and inhibits NO-stimulated phosphorylation of CREB. In postmortem temporal cortex from a series of AD patients there was reduced NO responsive sGC providing the first evidence for a loss of NO responsive sGC activity in AD brain. Alternatively, current research suggests S-nitroslylation, may be responsible for cGMP independent mechanisms of NO and can contribute to neurotoxicity in neurogenerative diseases such as AD. Consequently, NO does not always protect against disease and may help facilitate neurode generative disorders through nitro~ative stress and dysregulation of production. A common theme in many neurodegenerative disorders is the finding of abnormal aggregates of misfolded proteins. Recent findings have implied that NO-related species may significantly participate in the . process of protein misfolding through protein. S-nitrosylation under degenerative conditions. Qu et al. demonstrate that Cdk5 activity, a cyclin dependent kinase responsible for neuronal functions, is regulated by S-nitroslylation. They found significantly increased S-nitrosylated Cdk5 (SNO-Cdk5) levels in postmortem human brain tissues of patients with AD compared to control brain tissue. Significantly, SNO-Cdk5 was not detectable in control human brains, thus indicating that measurable levels of SNO-Cdk5 are representative of a diseased state. Additionally, researchers reported that formation of SNO-Cdk5 contributes to NMDA-induced spine loss, neuronal damage, and to A~-induced loss of synaptic spines. In conclusion, the SNO-Cdk5 mediated pathway may contribute to the path agenesis of AD and serve as a uniq.ue therapeutic for restoring spine damage in AD and other neurodegenerative diseases. . 9 -\r Collectively, the literature demonstrates a critical role for NO in the development of AD. It appears that normal and sufficient NO production/availability can modulate and inhibit the expression and formation of A~ but once A~ beco~es present it further compromises NO activity. This creates a perpetual system ofNO insufficiency and a feed forward mechanism that lllay accelerate AD progression. The NO pathway (both cGMP and through S-nitrosylation) may be an important therapeutic target in preventing and treating mild cognitive impairment, as well as AD. In fact, a high nitrate diet has been shown to increase regional cerebr::t! blood flow to the frontal lobe in older patients. It appears that the inability to produce sufficient NO under the right preclinical conditions enhances the risk for a number of diseases that plague the older population. If true, then there exist an opportunity to intervene early during this process, implement strategies to restore NO homeostasis, and, perhaps, delay or prevent the onset and progression of certain diseases. This gradual loss ofNO activity with age can be sped up or slowed down based on individual lifestyle and diet. Adopting healthy habits such as a good diet and exercise can prolong the precipitous drop in NO production with age. To the contrary a poor dietalong with physical inactivity can accelerate the process and lead to a faster decline in NO production at a younger age. Therapeutic strategies directed at improving endothelial function or providing an alternative source of NO should be the primary focus because they may reduce the incidence of atherosclerosis or other diseases that occur with aging, even perhaps AD. The role of diet in the prevention and control of morbidity and premature mortality due to noncommunicable diseases has been well established by vast population-based epidemio logical studies carried out during the last decade. NO is essential for maintaining normal blood pressure, preventing adhesion of blood cells to the endothelium, and preventing platelet aggregation; it may, therefore, be argued that this single abnormality, the inability to generate NO, puts us at risk for diseases that plague us later in life, such as atherosclerosis, myocardial infarction, stroke, and peripheral vascular disease. Are dietary and nutritional strategies utilizing nitrite and/or nitrate to restore NO homeostasis the best approach? More clinical trials are needed to define the c.:mtl"xt for risks vs. benefit. Although modestly increased associations between consumption of foods containing nitrite and nitrate and certain cancers have been reported in some prospective epidemiologic studies, findings across studies have been largely inconsistent and equivocal and thus the overall burden of proof remains inconclusive. As with any therapy or treatment regimen, a risk benefit evaluation should be considered and understood for certain persons or patient populations. However, given the emerging data on the growing number of benefits from diets and foods enriched in nitrite and nitrate, we predict the qenefits will far outweigh any risks. What remains clear is developing strategies and new technologies designed to restore NO availability is essential for inhibiting the progression of certain common chronic diseases. NO is formed from L-arginine via the enzyme nitric oxide synthase or synthetase (NOS). These enzymes convert L - arginine into L -citrulline, producing NO in the process. Oxygen and different co factors such as FAD, FMN, heme and tetrahydrobiopterine are necessary which influence NO synthesis by this rection. The dysfunctional nitric oxide synthase (NOS) nitric oxide pathway is considered an early marker for various cardiovascular disorders. Decreased bioavailability of endothelial nitric oxide plays a crucial. role. in the development and progression of a number of human diseases. Endothelial dysfunction results from decreased nitric oxide production or increased degradation 10 of nitric oxide. In certain aspects endothelial dysfunction can be defined as the inability to generate NO. Endothelial dysfunction is a physiological dysfunction of normal biochemical processes carried out by the endothelium, the· cells that line the inner surface of all blood vessels including arteries and veins (as well as the innermost lining of the heart and lymphatics). Endothelial dysfunction is associated with several cardiovascular disorders, including atherosclerosis. Prior attempts to restore nitric oxide homeostasis have met significant challenges. L-arginine and antioxidant supplements have consistently failed in clinical trials. It is known that NOS enzymes produce nitric oxide by catalyzing a five electron oxidation of the guanidino nitrogen of Larginine. While nitric oxide is produced through oxidation of the semi-essential amino acid Larginine by NOS, the L-arginine-nitric oxide pathway is dysfunctional in patients with endothdial dysfunction. Thus, feeding the nitric oxide pathway through L-arginine supplementation is potentially both ineffective and detrimental through the production of superoxide instead of nitric oxide. Prior attempts to enhance nitric oxide production with organic nitrates such as nitroglycerin have faced challenges. Early entry therapy with organic nitrates do not significantly improve survival in myocardial infarction but increases the .beneficial effects of the Angiotensin Converting Enzyme (ACE)-inhibitor enalapril by 50%. Certain short-term experimental and clinical investigations suggest that nitrate tolerance induced by nitroglycerin is associated with toxic effects in the vasculature. Chronic and long-term organiC nitrate therapy has been associated with reduced survival when used in patients with coronary artery disease. Endothelial dysfunction induced by a continuous treatment with nitroglycerin may be an additional risk for: patients who receive continuous nitroglycerin to treat conditions such as unstable angina and acute heart failure. Previous studies have shown that nitrites widen blood vessels, but US researchers writing in Nitric Oxide: Biology and Chemistry, the peer-reviewed journal of the Nitric Oxide Society, say theirs was the first to find that nitrites also increase blood flow to the brain. Beetroot contains high concentrations of nitrates, which are converted into nitrites by bacteria in the mouth. Nitrites help open blood vessels in the body, increasing blood flow and oxygen to places lacking in oxygen.Beetroot is a dark red vegetable with an acquired taste which has been getting a lot of coverage in the news. It has been linked with better stamina, improved blood flood and lower blood pressure Most beetroot is round and red, but yellow, white and stripy versions are available.The beetroot taste is described as sweet, earthy and tender to eat. It is grown in the ground and is related to turnips, swedes and sugar beet. It contains potassium, magnesium, iron, vitamins A, B6 and C, folic acid, carbohydrates, protein, antioxidants and soluble fiber. Researchers have known for some time that juice may help lower blood pressure, but in 2010 UK researchers revealed that nitrate is the special ingredient in beetroot· which lowers blood pressure and may help to fight heart disease. 11 In a Queen Mary University of London study, healthy participants had to drink a glass of beetroot juice while others had a dummy (placebo) drink. Others took nitrate tablets.Blood pressure was lowered within 24 hours in people who took nitrate tablets and those who drank beetrootjuice.The researchers admitted to BootsWebMD that beetroot juice is a love it or hate it kind of drink, but found people in the study didn't mind it so much when they were drinking it every day.People with very high blood pressure can end up being on multiple tablets, so a more natural approach could prove popular if the initial research results are confirmed. The study wns funded by the British Heart Foundation and is published online in the American Heart Association journal Hypertension. Drinking beetroot juice increases blood flow to the brain in older people, which may be able to _fig~t_ the pr()gr_ession p_f_dementia,_a 2010 stuciy sngg~c;ted.Beetroot contains-high conccntratiuus of nitrates, which are converted into nitrites by bacteria in the mouth. Nitrites help open blood vessels in the body, increasing blood flow and oxygen to places lacking in oxygen. T.here are some interesting side effects of eating too much beetroot. It can tUrn urine pink, which can be mistaken for blood in the urine. If you get kidney stones because of too much calcium, you may be advised to cut down on oxalates in your diet. Beetroot is just one food which contains oxalates, which prevent calcium from being absorbed by your body allowing it to build up as stones in the kidney. The British Dietetic Association says beetroot contains flavonoids called anthocyanins which are responsible for the deep pigments. Anthocyanins, the BOA says, can help with recovery from the stress of exercise during training and competition as well as helping to counter the effects of pollution on the body. Hawthorn is a plant. The leaves, berries, and flowers of hawthorn are used to make medidne.Hawthorn is used for diseases of the heart and blood vessels such as congestive heart failure (CHF), chest pain, and irregular heartbeat. It is also used to treat both low blood pressure and high blood pressure, "hardening of the arteries" (atherosclerosis), and high cholesterol. So far, research suggests that hawthorn might be effective in treating congestive heart failure, but there hasn't been enough research on other heart-related uses to know if it is effective for them. Research suggests that hawthorn can .lower cholesterol, low density lipoprotein (LDL, or "bad cholesterol"), and triglycerides (fats in the blood). It seems to lower accumulation of fats in the liver and the aorta (the largest artery in the body, located near the heart). Hawthorn fruit extract may lower cholesterol by increasing the excretion of bile, reducing the formation of cholesterol, and enhancing the receptors for LDLs. It also seems to have antioxidant activity. L-citrulline is a naturally occurring amino acid found in food, such as watermelons, and also made in the body. Our bodies change L-citrulline into another amino acid called L-arginine and also to nitric oxide. L-citrulline might help increase the supply of ingredients the body needs to making certain proteins. It might also help open up veins and arteries to improve blood flow and reduce blood pressure. 12 --------------------- Vitamin Bl2, or cobalamin, is essential to a wide variety of critical body functions. We need B12 for nervous system health, cardiovascular health, energy production and longevity. Getting optimal amounts of this important nutrient can do great things for our minds and bodies, but unfortunately, many people aren't even getting the bare minimum.Vitamin B12 is an essential nutrient for the. human body. In its active form, it is a in ethyl group donor that is involved in energy production, homocysteine metabolism, nerve function and neurotransmitter production. Bl2 works with folate to create red blood cells and the protective coatine around nerve cells, to convert food to energy and to synthesize and repair DNA. Bl2 deficiency is not a symptom experienced only by the sick, malnourished and elderly. On the contrary, it affects millions of Americans, even those with healthy diets and lifestyles. A recent study conducted by Tufts University suggests that B 12. deficiency and insufficiency affect 64% . of peopl~ between the ages of 26 and 83, and that suboptimal levels are equally as common at every age. Clinical deficiency (serum levels below 148 pmol/L) affected 9%, or nearly one in ten people, out of 2,999 subjects. These dangerously low levels are known to cause nerve damage, cognitive decline, loss of memory, fatigue, and anemia, among other things. An additional 16% of subjects were verging on deficient (levels below 185 pmol/L), and 39% had levels in the lownormal range (below 258 pmol/L). According to a recent study published iri the September 2008 issue of Neurology, B 12 levels below 308pmol/L are associated with an increased risk of brain shrinkage and cognitive decline. Together, these two studies suggest that 56% of the population may experience neurological impairment as a result of low levels of B 12, without being diagnosed as B 12 deficient. One of vitamin B 12's many vital functions is the formation and maintenance of the outer layer of nerves, called the myelin sheath. The myelin sheath is the fatty insulation around nerve cells that protects neurons and allows them to properly conduct signals. Integrity of the myelin sheath is essential for healthy brain function and is dependent upon methylation reactions that require B 12. B 12 also influences the production of neurotransmitters that control memory, thinking, motor function and moods. · B 12 deficiency affects the nervous system first, by damaging the myelin sheath. and then the entire nerve cell. This damage can result in a host of neurological conditions including multiple sclerosis, neuropathy, impaired coordination and loss of vision, hearing and memory. Animal studies have revealed that the methyl form of vitamin B12 (methylcobalamin) promotes the regeneration of nerve cells. Limited human trials suggest a role for B12 in slowing the progression ofneurodegenerative disease and lessening pain associated with neuropathy. B12 deficiency can also result in elevated blood ievels of the amino acid metabolite homocysteine. Numerous studies have cited a correlation between elevated homocysteine and Alzheimer's, dementia, depression and overall cognitive decline. Vitamin B12 is needed to create red blood cells and to convert homocysteine to methionine. Both of these functions are critical to the health of the cardiovascular system. Deficiencies of B 12 can result in megaloblastic anemia, characterized by oversized, immature red blood cells, and buildup of homocysteine in the blood, a risk-factor for heart disease. 13 B 12 is essential for energy production in every cell ofthe body and has earned the nickname "the energy vitamin." Supplying our bodies with adequate amounts of B12 helps our cells derive energy from the proteins, fats and carbohydrates we eat. Bl2's role in me.tabolism impacts the function of every tissue in the body, including the muscles, the heart and the brain. Vitamin B12 is essential for the synthesis and repair of DNA and it supports healthy gene expression. Gene expression is the process by which our genetic material is used to generate biochemicals within the body, and it influences whether we wiil live long, healthy lives or will suffer from disease. Nutrients that affect gene expression have the ability to "tum on" genes that promote health while "turning off' those that undermine health. Though 012 does nut directly regulate gene expression, it plays an important role in the production and recycling of S-adenosyl methionir1e __ (~AIV1e ), .~biochemical that-reacts with DNA to turn-genes on or off. This reaction, caTfed methylation, is a natural reaction within our bodies that supports healthy gene expression. 'fherefore, supplementing with B12 supports the healthy replication and function of our genetic material. Vitamin B 12 is a product of bacterial fermentation and is found exclusively in animal products. Beef, poultry, fish, cheese and eggs are all good sources of B 12. Although an inactive analogue of vitamin B 12 is found in some plants like algae, this form is not used by our bodies. Absorption of B12 in the small intestine requires the help of a glycoprotein known as intrinsic factor. Intrinsic factor, secreted by the parietal cells in the stomach, has a low affinity for inactive B12 analogues found in plant foods. Ifthese inactive analogues are absorbed into the body, they are taken to the liver and then excreted in the feces and urine. The following categories, would likely to be benefited from supplementation: );>: A senior - an estimated 40% of seniors have low stomach acidity (atrophic gastritis), which is linked to impaired absorption ofprotein-bound vitamin B12, found in food. The unbound B 12 found in supplements is generally better absorbed. ~ A vegetarian or vegan- vegetarians often do not consume adequate food sources ofB12 and vegans do not consume any food sources ofB12 (plant sources are analogues and are not absorbed); studies have shown that up to 50% of vegetarians and 80% of vegans are deficient. · ~ A pregnant - pregnancy increases the demand for B 12 to create more blood cells and to nourish the baby's growing nervous system; B12 deficiency during pregnancy has been linked with neural tube defects. ~ A man with low sperm count or low motility - B12 supports healthy sperm cell replication. When given to men without B 12 deficiency, it has reportedly increased sperm count and motility. ~ An acid blocker- Use of proton pump inhibitors has been linked with Bl2 depletion. ~ A perso11 taking metformin- research has shown a correlation between metformin & B12 deficiency. As dosage and duration increased, so did risk ofB12 deficiency. ~ A person havingGI problems (H. pylori, stomach acid imbalances, Crohn's Disease, Gastric or Duodenal Ulcers, etc.)- these complications interfere with absorption; studies have found low B 12 levels in individuals with stomach and/or intestinal problems. ~ A postmenopausal woman: Bone health is a concern for all of us, but particularly for postmenopausal women, who are most likely to suffer from bone loss and osteoporosis. B 12 plays an important role in bone health via its role in homocysteine metabolism. 14 . . Women with homocysteine levels above 15. 1-1mol/L were found to have a 96% higher risk of low bone density than women with levels below 9 1-1mol/L. ~ To improve memory, mental clarity, mood or energy levels - B 12 supports all of these bodily functions. Cyanocobalamin and methylcobalamin are the two most common chemical forms of B12. Cyanocobalamin is B12 (cobalamin) bound to a cyanicie molecule while methylcobalamin is B12 bound to a methyl group. Both forms are produced synthetically. Methylcobalainin is considered an active form because it does not need to be converted iri the body before it can function as B12. Cyanocobalamin is riot an active form because it must be converted to methylcobalamin before it can function as Bl2. Another form of B12, called dibencozide (also known as agenosylcobalamin ), is.another active-form-of R l2. B12 comes in sublingual, pill and liquid form. Sublingual form (a tablet that dissolves under the tongue) is a popular method of oral administration because the B12 is absorbed directly into the bloodstream through the mouth, and does nqt require intrinsic factor. This may be beneficial for individuals with impaired digestion or inadequate intrinsic factor. Although many medical doctors give B12 injections, oral administration is equally as effective, even in the absence of intrinsic factor. Research has established that, in individuals with pernicious anemia (B12 deficiency symptom), the average absorption rate of cyanocobalamin is 1.2 percent for a wide range of doses. This means that the average person taking a daily dose of 250 icrograms would absorb 3 micrograms. Since the daily turnover rate of B12 is about 2 micrograms, 250 meg daily would be sufficient for many people. However, there is little risk in taking higher doses, up to 2,000 micrograms daily, and many people benefit greatly from amounts as high as. 5,000 micrograms per day or higher. Higher doses are generally more effective at replenishing diminished B12 stores rapidly. Several medical tests are available to assess the levels ofB12. These include: Serum B12 levels-the most common, but often inadequate test. -·· )' Holotranscobalamin II-can detect B12 deficiency in its earliest stages-low levels indicate that the B 12 stores are diminishing. ~ Serum levels or Urinary excretion of methylma:Ionic acid--elevated levels indicate that cellular insufficiency or deficiency has already manifested. ~ Serum levels of homocysteine--elevated levels indicate that cellular insufficiency or deficiency has already manifested. Limitations of testing: Serum B12·levels alone are inadequate to diagnose B12 deficiency and insufficiency. In the original Framingham Study, more ~han half of seniors with cellular B12 deficiency had serum B 12 levels considered normal. This finding can be attributed to 2 factors: 1. The clinical ranges for "normal" serum B12 in the United States are much too broad. While levels between 200 pmol/L and 300 pmol/L are considered normal in the U.S., individuals \Vith levels this low often have obvious B12 deficiency symptoms. In Japan and some European countries, the clinical cutoff for deficiency is between 370 and 407 pmol/L 2. A serum B12 test measures all circulating B12, but about 80% of this B12 is unavailable to most cells. A holotranscobalamin II test, on the other hand, measures the remaining 20% of circulating cobalamin that is attached to a carrier molecule, enabling it to reach the body's cells. 15 Levels ofholotranscobalamin can be low in individuals .with normal serum B12-a situation that results in cellular deficiency. Methylmalonic acid and homocysteine. are also indicators of cellular deficiency. These three functional metabolite tests are very important for accurately assessing B 12 levels in the body. The NHLBI Study: The Promise of New Medical Uses for Sodium Nitrite for Heart Attack and Organ Damage suggest that: Sodium nitrite, a naturally occurring chemical and common meat preservative, is only used medically to treat cyanide poisoning. Rut if the results of a new animal study hold up under further research in people, the chemical may one day be used to protect and preserve tissue and organ function after heart attack, high risk abdominal surgery, and organ transplantation. Tile _Tl_t!W St!.!dY was conducte