Plasma low-density lipoprotein cholesterol

Wang J, Freeman DJ, Grundy SM, Levine DM, Guerra R, Cohen JC. Linkage between cholesterol 7alpha-hydroxylase and high plasma low-density lipoprotein cholesterol concentrations. J Clin Invest 1998 101 1283-1291. 

Couture P, Otvos JD, Cupples LA, Wilson PW, Schaefer EJ, Ordovas JM. Association of the A-204C polymorphism in the cholesterol 7alpha-hydroxylase gene with variations in plasma low density lipoprotein cholesterol levels in the Framingham Offspring Study. J lipid Res 1999 40 1883-1889. 

Friedman, M., Fitch, T. E., Levin, C. E., Yokoyama, W. Ft. (2000a). Feeding tomatoes to hamsters reduces their plasma low-density lipoprotein cholesterol and triglycerides. J. Food Set, 65, 897-900. 

Medina MW, Gao F, Ruan W, Rotter JI, Krauss RM (2008) Alternative splicing of 3-hydroxy-3-methylglutaryl coenzyme A reductase is associated with plasma low-density lipoprotein cholesterol response to simvastatin. Circulation 118 355-362... 

Nasta et al. also tried to investigate the relationship between cholesterol and mood states in the initial puerperal period. Their results showed that reduced plasma cholesterol concentration was associated with major feelings of fatigue and depressed mood [79]. In addition, West et al. compared the effects of transdermal versus oral estrogens on the vascular resistance index, mean arterial pressure, serum lipid concentrations, norepinephrine, and left ventricular structure in 10 postmenopausal women. The results showed that oral and transdermal estrogen significantly decreased the vascular resistance index, mean arterial pressure, norepinephrine, and total and low-density lipoprotein cholesterol to a similar extent [80],... 

Low-fat, high-carbohydrate diets have been shown to lower plasma low-density lipoprotein (LDL) cholesterol levels. At the same time, these diets decrease anti-atherogenic high-density lipoprotein (HDL)-cholesterol, and increase concentrations of plasma triglycerides, lipoprotein[a] (Lp[a]), and small dense LDL, plus increasing insulin resistance. Overall, these changes are likely to increase the risk of coronary heart disease (Willett, 2002 Kris-Etherton et al., 2002 Sanders, 2003). 

The commonly recognized risk factors for atherosclerosis include increasing age, sex (males > females until menopause, after which the incidence is similar), serum lipid levels (increased total cholesterol and low-density lipoprotein cholesterol, decreased high-density lipoprotein cholesterol, etc.), diabetes melli-tus, hypertension, and obesity. Other less well recognized but very important risk factors include increased plasma homocysteine, fibrinogen, and coagulation factor VII increased blood hematocrit, leukocyte count (increased neutrophils), and C-reactive protein and clinical depression. 

In a cross-sectional study in 44 men, olanzapine had a worse metabolic risk profile than risperidone (444). The men (mean age 29 years) took olanzapine (n = 22 mean duration 18 months mean dose 13 mg/day) or risperidone (,n = 22 mean duration 17 months mean dose 2.8 mg/ day). Those who took olanzapine had significantly higher plasma triglyceride concentrations, significantly higher very low density lipoprotein cholesterol concentrations, a trend to a lower HDL cholesterol concentration, and a... 

The effects of palm oil on serum lipids and lipoproteins recorded in animal studies have similarly been observed in several human studies. In some early human studies (152, 153), it was reported that subjects on a palm oil diet had elevated plasma and low-density lipoprotein cholesterol LDL-C levels compared to a diet containing a polyusaturated fat. However, on a critical reassessment of these and other relevant studies (154), it was found that plasma cholesterol levels after the palm oil period were actually lower than at the point of entry of the experiments when the subjects were on their habitual diets. 

The typical sunflower oil composition is 66-72% linoleic acid, 12% saturated acids (palmitic and stearic), 16-20% oleic acid, and less than 1% a-linolenic acid. An increase in low-density lipoprotein cholesterol (LDL-C) and a decrease of high-density lipoprotein cholesterol (HDL-C) are believed risk factors of coronary heart disease (CHD). Diets rich in saturated fat increase plasma total and LDL-C. Traditional high-linoleic sunflower oil has always been regarded as healthy because of its high content of polyunsaturated fatty acids (PUFA) and relatively low content in saturated fatty acids. 

Ishikawa et al. (70), in a double-blind, cross-over trial in hypercholesterolemic patients, demonstrated that GLA lowered low-density lipoprotein cholesterol and apolipoprotein B in plasma and increased HDLC levels without affecting the levels of total cholesterol. Jantti et al. (71) observed a decrease in plasma... 

DeLong DM, DeLong ER, Wood PD, Lippel K, Rifkind BM. A comparison of methods for the estimation of plasma low- and very low-density lipoprotein cholesterol. The Lipid Research Clinics Prevalence Study JAMA 1986 256 2372-7. 

Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Chn Chem 1972 18 499-502. 

In patients with renal insufficiency and urinary protein excretion greater than 3 g/day, the major lipid abnormalities are elevations of plasma total and low density lipoprotein cholesterol (prevalence 85% to 90%), with approximately 50% of patients experiencing a low level (<35 mg/dL) of high density lipoprotein (HDL) cholesterol, and 60% of patients showing triglyceride concentrations greater than 200 mg/dL. ... 

Fatty acids affect CHD risk, in part, via effects on plasma lipids and lipoproteins. A meta-analysis of 60 controlled trials (Mensink et al., 2003) reported that saturated and trans fatty acids increase low-density lipoprotein cholesterol (LDL-C), whereas unsaturated fatty acids decrease LDL-C. Saturated fatty acids, MUFA, and PUFA all increase high-density lipoprotein cholesterol (HDL-C), whereas trans fatty acids do not. Both MUFA and PUFA decrease the TC to HDL-C ratio, whereas trans fatty acids increase it, and SFA have little effect (Fig. 20.4). 

Thyroid hormones regulate the turnover of carbohydrates, lipids, and proteins. They promote glucose absorption, hepatic and renal gluconeogenesis, hepatic glycogenolysis, and glucose utilization in muscle and adipose tissue (18). They increase de novo cholesterol synthesis but increase low-density lipoprotein degradation and cholesterol disposal even more, leading to a net decrease in total and in low-density lipoprotein cholesterol plasma levels (19). Thyroid hormones are anabolic when present at normal concentrations they then stimulate the expression of many key enzymes of metabolism. ... 

Abbey, M., Noakes, M., Belling, G.B., and Nestel, P.J., Partial replacement of saturated fatty acids with almonds or walnuts lowers total plasma cholesterol and low-density-lipoprotein cholesterol, Am. J. Clin. Nutr., 59, 995-999, 1994. 

Friedewald, W.T., Levy, R.I., and Fredrickson, D.S. (1972) Estimation of the Concentration of Low-Density Lipoprotein Cholesterol in Plasma, Without Use of the Preparative Ultracentrifuge, Clin. Chem. 18,499-502. 

Millions of people in the world suffer from cardiovascular disease, and it is a leading cause of death in both men and women. Elevation in plasma low-density lipoprotein (LDL) cholesterol levels is a major risk factor for myocardial infarction (heart attack) in these patients. Drugs to reduce dyslipidemia have included niacin and the fibrate class, but each of these has clinical limitations, such as low efficacy or toxic side effects. The development of HMG-CoA reductase inhibitors, or statins, has had an enormous clinical impact on the treatment of heart disease and prevention of heart attack, and these are taken by tens of millions of patients worldwide [1]. One of the first such drugs, lovastatin, was discovered in the 1970s as a fungal natural product [2] and lowered lipid levels in animals and healthy volunteers. Problems with the development of another early statin, compactin, halted advancement of lovastatin to regular clinical use until the late 1980s. Since then. 

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