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Red yeast rice may lower blood lipid levels

January 25, 2010 by · Leave a Comment 

CM NEWS – Replacing daily intake of white rice with red yeast rice may have a positive lipid-lowering effects in patients with primary hyperlipidemia, a meta-analysis of 93 randomized trials concludes.

The study was released in Chinese Medicine journal and was a joint study by alternative medicine experts in Norway and traditional Chinese medicine researchers in Shanghai and Beijing.

The meta study analyzed data from 93 randomized trials which include a total of 9625 participants. Researchers find that hyperlipidemia patients who have consumed red rice show significant reduction of serum total cholesterol levels (weighted mean difference -0.91 mmol/L, 95% confidence interval -1.12 to -0.71), triglycerides levels (-0.41 mmol/L, -0.6 to -0.22), and LDL-cholesterol levels (-0.73 mmol/L, -1.02 to -0.043), and increase of HDL-cholesterol levels (0.15 mmol/L, 0.09 to 0.22), compared to placebo groups.

Researchers emphasize that the positive effect on lipid levels by red rice shown by these studies indicates short term benefits. Whether red rice should be recommended as an alternative treatments for primary hyperlipidemia requires further studies.

According to Medline, red yeast rice contains several compounds collectively known as Monacolins, substances known to inhibit cholesterol synthesis. One of these, “Monacolin K” is a potent inhibitor of HMG-CoA reductase, and is also known as Mevinolin or Lovastatin (Mevacor®, a drug produced by Merck & Co., Inc).

Medline also says:

There is limited evidence about the side effects of red yeast. Mild headache and abdominal discomfort can occur. Side effects may be similar to those for the prescription druglovastatin (Mevacor®). Heartburn, gas, bloating, muscle pain or damage, dizziness, asthma, and kidney problems are possible. People with liver disease should not use red yeast products.

In theory, red yeast may increase the risk of bleeding. Caution is advised in patients with bleeding disorders or taking drugs that may increase the risk of bleeding. Dosing adjustments may be necessary. A metabolite of Monascus called mycotoxin citrinin (CTN) in fermentation may be harmful.

Garlic lowers blood glucose levels of diabetics, helps hypertension

January 25, 2010 by · Leave a Comment 

CM NEWS – Garlic may restore some of the antioxidants damaged by free radicals in patents with vascular diseases such as diabetes and hypertension, according to a new study.

The study is recently published by the Evidence-based Complementary and Alternative Medicine. Rats induced to have diabetes and hypertension were given an an aqueous extract of garlic (500 mg/kg IP daily) for 3 weeks.

As a result, the blood antioxidant levels of these rats after 3 weeks of treatment were significantly higher (P < 0.001) than the pretreatment levels in both diabetic and hypertensive rats. The increased serum antioxidant levels were paralleled by a decrease in serum glucose in the garlic-treated diabetic rats and lowered systolic blood pressure in the garlic-treated hypertensive rats.

What is the importance of antioxidants? Oxidative stress, an excessive production of reactive oxygen species (ROS) above the body’s antioxidant capacity, has been implicated in the development of many pathophysiological conditions including hypertension, diabetes, atherosclerosis and cancer, as well as the process of aging.

ROS are normal products of cellular metabolism which are usually removed by endogenous antioxidants. However, it has become increasingly clear that overproduction of ROS can lead to a damaging cycle of lipid peroxidation, depletion of natural antioxidants such as glutathione, perturbation of nitric oxide production and disruption of normalcellular metabolism. These changes have been shown to cause damage to cell membranes and in particular can cause endothelial dysfunction.

During the last decade, it has become increasingly evident that many chronic diseases are accompanied by increased levels of oxidative stress exacerbated by decreased antioxidant levels. These observations have precipitated much interest in study of the correlations between oxidative stress, antioxidant potential and development of chronic diseases in both humans and animal models. Of particular interest are the correlations between oxidative stress and development of diabetes and hypertension.

The researchers conclude that treatment of diabetic rats with garlic resulted in significantly increased antioxidant and lowered glucose levels compared to untreated diabetic animals.

Haemostasis or normal blood clotting is essential for survival

September 5, 2009 by · Leave a Comment 

From public health scares about the risk of deep vein thrombosis (DVT) on long-distance flights to high rates of pulmonary embolism (PE) in patients recovering from major surgery, venous thromboembolism (VTE) is a well-publicised, serious health issue.1, 2
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Patients undergoing major orthopaedic surgery for total hip or total knee replacement or surgery for fracture of the hip are at particularly high risk of DVT. Undertreatment remains a problem, despite ample evidence that primary preventive therapy effectively reduces the risk of DVT, PE, and fatal PE.3, 57

Thrombosis complications also play a major role in cardiovascular disease. Blood clots in coronary arteries cause acute coronary syndrome, and blood clots that form in the heart are the major cause of stroke in people with atrial fibrillation.4, 5

The normal physiological response that prevents significant blood loss following vascular injury is called haemostasis.6 Familiarity with haemostasis lays the groundwork for a thorough understanding of the major disease states associated with thrombosis, such as venous thromboembolism (VTE), atherothrombosis (thrombosis triggered by plaque rupture), and cardioembolic stroke.
Blood vessel injury triggers the following sequence:

  • The vessel constricts to reduce blood flow
  • Circulating platelets adhere to the vessel wall at the site of trauma
  • Platelet activation and aggregation, coupled with an intricate series of enzymatic reactions involving coagulation proteins, produces fibrin to form a stable haemostatic plug

This finely tuned process serves to maintain the integrity of the circulatory system.10 However, the process can go out of balance, leading to significant morbidity and mortality.11

Vessel wall chart: clot initiation, formation and fibrinolysis Coagulation schematic

Abnormal haemostasis

Excessive coagulation leads to the formation of a thrombus, potentially obstructing blood flow. This is a common problem, especially in hospitalised or immobilised patients. Venous thromboembolic disease, for example, is a major problem in the European Union, where it causes more than one million events or deaths every year.12

Excessive bleeding results when certain coagulation factors are lacking, as in patients with haemophilia.13


The coagulation cascade

Coagulation involves a complex set of protease reactions involving roughly 30 different proteins.14 The final result of these reactions is to convert fibrinogen, a soluble protein, to insoluble strands of fibrin. Together with platelets, the fibrin strands form a stable blood clot.

An evolving model

For decades, the coagulation cascade was conceptualised as having two distinct points of initiation, labelled the extrinsic and intrinsic pathways.15 Over time, however, it has become clear that these pathways do not function in the body as parallel, independent systems.

The finding that the tissue factor-factor VIIa complex from the extrinsic pathway activates factors in both systems suggests that they are linked. This discovery, combined with an evolving understanding of the role of different cells, in particular blood platelets, has led to a cell-based model of coagulation. Unlike the older, intrinsic/extrinsic cascade model, the cell-based model includes the important interactions between cells directly involved in haemostasis (ie, tissue factor-bearing cells and platelets) and coagulation factors. This model more accurately represents the interaction between cellular activity and coagulation proteins that leads to blood clot formation.15

The intrinsic and extrinsic pathway model

This model divides the initiation of coagulation into distinct parts: the extrinsic pathway and the intrinsic pathway.6 The extrinsic pathway is the primary initiator of coagulation, while the intrinsic pathway leads to the successive activation of Factors IX and X. Activated Factor X (Factor Xa) plays a central role in the coagulation cascade, as it occupies a point where the intrinsic and extrinsic pathways converge.

The cell-based model

The cell-based model identifies the membranes of tissue factor–bearing cells and platelets as the sites where activation of specific coagulation factors occurs.15 This model posits a three-phase process — initiation, amplification, and thrombin action. Initiation occurs after vascular injury, when tissue factor–bearing cells bind to and activate Factor VII. This leads to production of a small amount of thrombin. Thrombin then activates platelets and cofactors during the amplification phase. The prothrombinase complex (comprising Factor Xa and cofactors bound to activated platelets) is responsible for the burst of thrombin production leading to the third phase of clot formation.

Propagation of clotting: the central role of Factor Xa

Factor Xa plays a central role in the coagulation process in both the older, extrinsic/intrinsic model as well as the more recently proposed cell-based model.

The coagulation cascade is triggered when injury to a blood vessel allows blood to come in contact with tissue factor (TF)–bearing cells. Factor Xa, with activated Factor V (Va) as a cofactor, propagates coagulation by converting prothrombin (Factor II) to thrombin (Factor IIa).15 Factor Xa is the primary site of amplification in the process: one molecule of Factor Xa catalyses the formation of approximately 1000 thrombin molecules.16 For this reason, development of medications that inhibit Factor Xa is an active and promising area of pharmaceutical research.17

Final step: fibrin formation

In the final step of the series of protease reactions leading to clot formation, thrombin triggers conversion of the soluble protein fibrinogen to insoluble fibrin strands. Thrombin also activates Factor XIII, which stabilises the clot by cross-linking the fibrin. The resulting fibrin mesh traps and holds cellular components of the clot (platelets and/or red blood cells).6

Fibrinolysis: restoring blood flow

Fibrinolysis, as the term implies, is the process that dissolves fibrin. It leads to clot dissolution. Plasminogen is the precursor of plasmin, which breaks up fibrin clots. During initial clot formation, plasminogen activators are inhibited. Over time, endothelial cells begin to secrete tissue plasminogen activators to start dissolving the clot as the structural integrity of the blood vessel wall is restored. Medications that convert plasminogen to plasmin are used to treat acute, life-threatening thrombotic disorders, such as myocardial infarction.6

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