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Dyslipidemia is a major cause of atherosclerosis and atherosclerosis-associated conditions, such as coronary heart disease (CHD), ischemic cerebrovascular disease and peripheral vascular disease. Both genetic disorders and lifestyle contribute to the dyslipidemia seen in developed countries around the world (Goodman and Gillman, 2006). Dyslipidemia is the most common cause of death in both Western and Eastern societies (Epstein, 1992). There is no natural cut off between normal and abnormal lipid levels because lipid measurements are continuous. Diet rich in cholesterol and saturated fats contribute to the elevation of lipid levels in blood and to the progression of atherosclerosis. Epidemiological observations have shown that there is a strong positive Correlation between the concentration of circulating cholesterol, specifically the LDL cholesterol fraction and the risk of atheroma. (Watson et al 1995)
Approximately two thirds of cholesterol circulating in the blood is made up of liver. Hepatocyte synthesizes cholesterol and bile acids from acetate, and secretes them in bile where they are involved in fat absorption. The rate limiting enzyme in the cholesterol biosynthesis is the 3-hydroxy 3-methyl glutaryl Co-enzyme A (HMG CoA) reductase. Fats absorbed in the form of TG -rich chylomicrons and free fatty acids are cleaved from TG by lipoprotein lipase (LPL), an enzyme on the surface of the endothelial cells. Chylomicrons remnants are taken up by hepatocyte to complete the exogenous cycle. The endogenous cycle consists of secretion of TG rich lipoprotein particles (VLDL) that also contain cholesterol, by the liver into blood, followed by the removal of the free fatty acids by LDL in the capillaries. This will be showed in progressive enrichment of the particles with cholesterol increase in the liver density through intermediate density lipoprotein (IDL) to low density lipoprotein (LDL). HDL cholesterol dose not cause such problems, because, unlike LDL cholesterol, it favours the delivery of excess cholesterol from peripheral sites to the liver for elimination. The mechanisms for the protective effect of HDL cholesterol against atherosclerosis are unknown. But it may relate to the action of HDL cholesterol in the reverse cholesterol transport or to its ability to act as an antioxidant and has been shown to inhibit lipid peroxidation. HDL cholesterol contains platelets activating factors acetyl hydrolase and paraoxonase enzymes, which may protect against the formation of biologically active oxidised LDL particles. These contrasting mechanisms provide a rationale for the association of risks for coronary heart disease with high LDL levels and low HDL levels.
There is strong and positive association between total and LDL cholesterol and risk of cardiovascular events extending over a wide range of cholesterol concentration. The association applies to individuals with or without established CVD as well as to women and men .other risk factor can substantially aggravate the effects of LDL cholesterol. The result of epidemiological studies, as well as trials with angiographic or clinical end points confirms the importance of LDL in the pathogenesis of atherosclerosis. There is also strong and inverse association between HDL cholesterol and risk of CVD in both men and women and in subjects with or without established CVD; the lower the concentration of HDL cholesterol the greater the risk of CVD.
A linear relation probably exists between lipid levels and cardiovascular risk, so many people with "normal" cholesterol levels benefit from achieving still lower levels. Consequently, there are no numeric definitions of According to National Commission on Macroeconomics and Health (NCMH), India, there would be around 62 million patients with Coronary Heart Disease by 2015 in India and of these; 23 million would be patients younger than 40 years of age (Chaturvedi and Bhargava, 2007).
It has been pointed out that postprandial hyperlipidemia accelerates arteriosclerosis. A strong relationship exists between insulin resistance or glucose intolerance and postprandial hyperlipidemia (Masumi et al., 2007). Among them, postprandial increase in remnant lipoproteins (RLP) has been recognized as a powerful CHD risk factor not only for diabetic but also for non diabetic subjects (Karpe et al., 2001). This relationship is non-linear and depends strongly on the presence of the other risk of atheroma. This relationship is non liner and depends strongly on the presence of other risk factors including male sex, arterial hypertension, cigarette smoking, diabetes mellitus and positive familial or personal history of ischaemic heart disease familial or personal history of ischaemic heart disease, electrocardiographic and echocardiographic observations.
The statins are the most effective and best-tolerated agents for dyslipidemia, by Inhibition of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, which catalyses an early, rate-limiting step in cholesterol biosynthesis. The most common side effect of these potent statins is the loss of muscle function, muscle pain and cramps. The problems get exacerbated for older patients (over the age of 50) who have complained of debilitating pain to the point that no movement is possible. In some cases severe neuromuscular degeneration has resulted with symptoms similar to multiple sclerosis (Goodman and Gillman, 2006).
There are various natural herbs that effectively lower cholesterol without any side effects. There are estimated to be around 25,000 effective plant-based formulations, used in folk medicine and known to rural communities in India (Kamboj, 2000). Out of which, 166 different species of plants are used in the Ayurvedic Pharmacopoeia as antihyperlipidemic agents (Khan and Michael, 2001). Although several chemical and drugs generally used to lower blood lipid and atherogenesis the drugs of plant origin receives considerable attention to re-establish traditional claims with scientific interest (Tanner et al., 1991).
Herbs are mines of medicinal agents the need for research is required to find efficacious cheap and safe hypolipidemic agent from among the natural products (Prithviraj and Mishra, 2000). Medicinal plants may produce several biological activities in humans, generally very little is known about their toxicity (Sateesh and Adepalli, 2009). In order to access the toxicity of antihyperlipedimic plant toxicity study was carried out. Toxicological study involves two phase: first phase acute toxicity and second phase chronic toxicity study. The major objective of the second phase study is the final prediction of the safe starting dose definition of the safe specific organ toxicity likely to be encountered in the patients. With this criteria; efforts to develop effective and better antihypolipidemic herbal plant and toxicity study of the plant.
The use of herbs as medicines is as old as history itself. Some authors state that the first recorded use of herbs for medicinal treatment began over 4000 years ago. Traditional Indian Medicine has been dated back to 3000 B.C. One form of Traditional Indian Medicine is called Ayurveda. This type of medicine places a heavy emphasis on the use of herbs for the treatment of various ailments. A combination of European, Chinese, Ayurvedic, and other unconventional treatments influenced the use of herbs to the present day (Richard, 2009). India has one of the richest plants medical traditions in the world. As per the available records, the herbal medicine market in 1991 in the countries of the European Union was about $ 6 billion (may be over $20 billion now), with Germany account for $3 billion, France $ 1.6 billion and Italy $ 0.6 billion. In 1996, the US herbal medicine market was about $ 4 billion, which have doubled by now. The Indian herbal drug market is about $ one billion and the export of herbal crude extract is about $80 million (Evan, 1994).
Fructose feeding a model of hyperlipidemia hyperglycemias and insulin resistance through the elevated synthesis of cholesterol, fatty acid and triglyceride in liver.(Goyal et al., 2007). (sedentary behaviour and diets high in calories, saturated fat, and cholesterol)
Obesity and type 2 diabetes are occurring at epidemic rates in the United States and many parts of the world. The "obesity epidemic" appears to have emerged largely from changes in our diet and reduced physical activity. An important but not well-appreciated dietary change has been the substantial increase in the amount of dietary fructose consumption from high intake of sucrose and high fructose corn syrup, a common sweetener used in the food industry. A high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, perturbs glucose metabolism and glucose uptake pathways, and leads to a significantly enhanced rate of de novo lipogenesis and triglyceride (TG) synthesis, driven by the high flux of glycerol and acyl portions of TG molecules from fructose catabolism. These metabolic disturbances appear to underlie the induction of insulin resistance commonly observed with high fructose feeding in both humans and animal models. Fructose-induced insulin resistant states are commonly characterized by a profound metabolic dyslipidemia, which appears to result from hepatic and intestinal overproduction of atherogenic lipoprotein particles. Thus, emerging evidence from recent epidemiological and biochemical studies clearly suggests that the high dietary intake of fructose has rapidly become an important causative factor in the development of the metabolic syndrome. There is an urgent need for increased public awareness of the risks associated with high fructose consumption and greater efforts should be made to curb the supplementation of packaged foods with high fructose additives. The present review will discuss the trends in fructose consumption, the metabolic consequences of increased fructose intake, and the molecular mechanisms leading to fructose-induced lipogenesis, insulin resistance and metabolic dyslipidemia. (Heather et al., 2005)
Heather Basciano, Lisa Federico and Khosrow Adeli. Fructose, insulin resistance, and metabolic dyslipidemia. Nutrition & Metabolism 2005, 2:5