Raising Low HDL Essay Example | Topics and Well Written Essays - 1250 words

Raising Low HDL - Essay ExampleThe pathological epitome in an atherosclerotic lesion suggests accumulation of LDL and its oxidization in the vascular subendothelial space, where monocytes from the circulation enter to initiate an incitive reaction that would lead eventually to atheroma formation. Research has also demonstrated that monocyte entry occurs at the sites of LDL peroxidation, suggesting that oxidation is the cause of monocytes entry. Research has also shown that HDL apoA-I and apoA-I representational peptides get to been shown to prevent LDL oxidation. Moreover, HDL apoA-I and apoA-I mimetic peptides have been shown to decrease atherosclerotic lesions and improve vascular reactivity in humans. Regarding its mechanism of action in producing beneficial effects against atherogenesis, studies have suggested that HDL enhances the reverse cholesterol transport. Over the top of it, apoA-I is also undefendable of scavenging the seeding molecules from LDL, thus preventing the LDL-derived phospholipid oxidation and the inflammatory response out of the byproducts. Thus, clinical managements directed towards improving the HDL cholesterols in the body could result in a therapeutic option of prophylactic potential in persons who be prone to atherosclerosis due to lifestyle reasons of high cholesterol and high triglycerides (Navab, M et al., 2004). Consequently, there be many therapeutic options available to enhance the HDL in human beings, and they are Fibrates, Niacin, and recently lean oils containing omega-3 fatty acids. All of them are recommended however, given the volume of evidence, it is very difficult to create a guideline for the patients. This work intends to critically review contemporary literature to compare the findings so a iodin agent can be chosen based on evidence in order to agitate the HDL levels in blood.Fibrates While statins are regarded as therapeutic cornerstones in dyslipidemia, they are ineffective because they have proven ef ficacy in reducing the plasma levels of LDL-C. However, they are incompetent is reducing the elevated concentrations of triglyceride productive lipoproteins, VLDL and VLDL remnants, and they have minimal actions in increasing the low levels of HDL-C that are protective. Fibrates have been detect to reduce plasma levels of triglycerides by 30-50% and typically cast up levels of HDL-C by 5-15%, depending on lipid phenotype and baseline concentration. Fibrates may also reduce LDL-C potentially by up to 15-20% although the effect is variable, depending on the underlying lipid abnormality and baseline lipid phenotype (Chapman, MJ., 2006). This indicates individuals treated with Fibrates, levels of LDL would decrease when their plasma concentrations are elevated and HDL-C levels will increase when baseline plasma concentrations are low. Moreover, it efficiently reduces apoIII-C containing lipid particles which are acknowledged to be markers of change magnitude risks for atherogenesi s. The increased HDL levels following Fibrates are generally reflected by increased plasma levels of apoA-I and apoA-II. The Fibrates act via activation of a nuclear transcription factor PPAR in vascular tissues that actively metabolize lipids. This can be apply for both primary prevention and secondary prevention of atherosclerotic cardiovascular disease with demonstrably substantive decrease in the rates of