Clin Pharmacol Ther
August 2018
Genetic, metabolic, and lifestyle modifications can cause elevations of lipoproteins that contribute to atherosclerotic lesions over time. In the modern world with life extension from many improvements in medicine and public health, most humans live long enough to develop atherosclerosis with concentrations of blood plasma lipoproteins that are very common. Familial abnormalities are prevalent and provide additional challenges in identifying unhealthy but treatable values of low-density (LDL) and very low-density lipoproteins (VLDL).
View Article and Find Full Text PDFPlasma triglyceride concentrations are normally below 150 mg/dL in the fasting state. However, these lipids can reach values of several thousand mg/dL. Elevations in this range are due to a massive retention of chylomicrons and usually result from multiple genetic variants with superimposed influences such as diabetes and immune disorders.
View Article and Find Full Text PDFThe measurement of cholesterol and triglycerides as indicators of metabolic disorders and most particularly of vascular disease risk has been of growing importance to physicians and epidemiologists over the past century. This was refocused on the lipoproteins, the specific packages in blood that carry these lipids, by John Gofman, MD, PhD, and Don Fredrickson, MD, more than 50 years ago. We continue to learn about the metabolism of these large molecular structures and their relationship to arteriosclerosis as new genetic and interventional studies are published.
View Article and Find Full Text PDFOvarian failure occurs in most women during the late fifth decade or early sixth decade of life. This causes a number of changes in physiology as estrogen and progestin concentrations decline. These involve lipoprotein metabolism and the vasculature.
View Article and Find Full Text PDFThe measurement of cholesterol and triglycerides as indicators of metabolic disorders and most particularly of vascular disease risk has been of growing importance to physicians and epidemiologists over the past century. This was refocused on the lipoproteins, the specific packages in blood that carry these lipids, by John Gofman, MD, PhD, and Don Fredrickson, MD, more than 50 years ago. We continue to learn about the metabolism of these large molecular structures and their relationship to arteriosclerosis as new genetic and interventional studies are published.
View Article and Find Full Text PDFThe roundtable discussion in this issue will focus on the problems faced by young women with lipid disorders. This is often the source of confusion for the patient and physician because the myth continues that young women do not have complications of atherosclerosis as a result of elevated blood cholesterol. The essential role of women in bearing children during the early years of adulthood also produces difficult decisions because the mother and fetus are usually experiencing similar exposure to therapeutic regimens.
View Article and Find Full Text PDFLipodystrophy comes in several forms, some involving the complete failure to develop adipose tissue and others with a partial absence in various bodily distributions. All appear to have a major genetic basis, and all involve a high frequency of lipoprotein disorders. High triglycerides and low high-density lipoprotein cholesterol are the usual findings that raise interesting questions as to how such abnormalities characteristic of obesity can be caused by genetic variants that produce a paucity of adiposity.
View Article and Find Full Text PDFBecause the Human Genome Project reached its first major milestone in completing the full sequence of human DNA, many new discoveries have been made relating genetic variants to disease. The new methodology that allows much more rapid and focused analyses of selected genes and the ability to screen the entire exome of any individual has provided tools to examine literally thousands of individuals for a given study. Genetic analysis has become a large-scale epidemiologic tool for examining variants in gene structure and correlating them with phenotypic markers of human disorders.
View Article and Find Full Text PDFPurpose Of Review: To examine the evidence for the adverse effects that have been reported during the use of statins.
Recent Findings: We now have over twenty years of prescription use and many large well controlled trials with statin therapy for hypercholesterolemia. There is only one significant and well documented adverse effect with this group of drugs, rhabdomyolysis.
J Clin Lipidol
March 2007
High-density lipoproteins (HDL) contain approximately 25% of the cholesterol and <5% of the triglyceride in the plasma of human blood. However, the dynamic exchange of lipids and lipid-binding proteins is not revealed by simply considering the mass of material at any point in time. HDL are the most complex of lipoprotein species with multiple protein constituents, which facilitate cholesterol secretion from cells, cholesterol esterification in plasma, and transfer of cholesterol to other lipoproteins and to the liver for excretion.
View Article and Find Full Text PDFStroke is one of the leading causes of death in the United States and worldwide. Metabolic syndrome, comprising abdominal obesity, elevated triglyceride levels, low levels of high-density lipoprotein cholesterol, elevated blood pressure, and impaired glucose metabolism, greatly increases the risk of cardiovascular disease, including stroke. The high prevalence of metabolic syndrome among individuals who experience stroke makes the metabolic syndrome a target for aggressive intervention and therapy.
View Article and Find Full Text PDFPurpose Of Review: The design, process and outcomes are compared between two large clinical trials of LDL cholesterol reduction with statin treatment in patients with known high blood pressure. This new information is placed in the context of previous clinical trials of cholesterol reduction, which have provided analyses of sub-groups with high blood pressure.
Recent Findings: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial failed to find a significant reduction of total mortality (primary endpoint), cardiovascular mortality or major cardiovascular events.