| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Lowering cholesterol in old age Oliver, M. F. (1999), J R Coll Physicians Lond 33(3): 252-3. Abstract: In arguing for a conservative view of the need for and wisdom of lowering plasma cholesterol, or low density lipoprotein cholesterol, in advanced age, three considerations are taken into account. These are: plasma cholesterol concentrations decrease spontaneously with age, as does their association with vascular disease; the absence of data to demonstrate the benefits of lowering cholesterol levels in the elderly; and conflicting priorities (including the cost of treatment) in the care of the elderly. Patients with known coronary heart disease who have received lipid-lowering treatment for some years could continue to be treated with these drugs beyond the age of 75, though even this decision should depend on clinical judgement. |
| Lowering cholesterol naturally Nash, D. T. (1990), Postgrad Med 87(2): 63-5, 68. Abstract: Patients today are more likely than ever to seek advice about reducing cholesterol levels. Physicians can help by teaching patients how to cut down on saturated fats. However, as Dr. Nash points out, eating habits are difficult to change, especially for those who think that healthy foods have an unpleasant taste. This article discusses several dietary interventions that have been proven to reduce cholesterol levels and thus the risk of coronary artery disease. |
| Lowering cholesterol with Anticholest--a high fiber guar-apple pectin drink Pirich, C., P. Schmid, et al. (1992), Wien Klin Wochenschr 104(11): 314-6. Abstract: In order to determine the efficacy of Anticholest, an apple-pectin-guar soft-drink in reducing elevated cholesterol (c) levels, 33 participants (aged from 8 to 73 years) were divided into three groups of comparable age, body-mass index, total c, LDL-c, HDL-c, and triglycerides. They received this combined fiber product either (group 1) at dosages of 1 cup (17 g) every second day, or (group 2) of 1 cup a day or (group 3) of 2 cups a day. Anticholest significantly reduced total c, LDL-c and the total c/HDL-c ratio. In group 3 HDL-c was increased significantly (p less than 0.01). The average percentage decrease in total c was 10.0% for group 1, 10.7% for group 2, and 15.7% for group 3. LDL-c was lowered 14.4% in group 1, 13.8% in group 2 and 19.1% in group 3. The highest individual reduction amounted to more than 30% for total-c and LDL-c. A significant decrease was also detected in the triglycerides (tg) in group 3 (p less than 0.05). 7 patients were non-responders. Anticholest appears to be an appropriate treatment for patients at risk of coronary heart disease with insufficient or inadequate response to dietary measures, but where long-term pharmacotherapy is not yet indicated. The lack of side effects and its form of administration as a viscous drink are important determinants for long-term compliance, which is essential in the management of a chronic progressive disease such as atherosclerosis. |
| Lowering cholesterol with drugs and diet Pedersen, T. R. (1995), N Engl J Med 333(20): 1350-1. |
| Lowering cholesterol: effects on trauma death, cancer death and total mortality MacMahon, S. (1992), Aust N Z J Med 22(5 Suppl): 580-2. Abstract: Randomised trials of cholesterol reduction (26 trials, 50,000 patients, net cholesterol reduction approximately 10%) have demonstrated a clear reduction in the incidence of coronary heart disease (CHD) after just a few years of treatment. Overall, the reduction in CHD death was only half as large as the reduction in non-fatal myocardial infarction (MI), although both were statistically significant (2P < 0.005). In these trials, 60% of all deaths were from CHD, and since treatment reduced these by about 10%, the expected reduction in total deaths was about 6%. This expected reduction falls within the 95% confidence interval of the observed effect of cholesterol reduction on total mortality in these trials. There were small excesses of deaths from cancer and deaths from trauma among patients allocated active treatment. However, in no single trial, nor in the trials collectively, were these increases statistically significant. Furthermore, the increases did not appear to be specific to any one agent nor were the increases consistent between trials of the same agent. These observations are consistent with the hypothesis that the small excesses of cancer and trauma deaths observed in the cholesterol reduction trials occurred by chance. |
| Lowering effect of dietary milk-whey protein v. casein on plasma and liver cholesterol concentrations in rats Zhang, X. and A. C. Beynen (1993), Br J Nutr 70(1): 139-46. Abstract: The effect of dietary whey protein v. casein on plasma and liver cholesterol concentrations was investigated in female, weanling rats. Balanced, purified diets containing either whey protein or casein, or the amino acid mixtures simulating these proteins, were used. The high-cholesterol diets (10 g cholesterol/kg feed) had either 150 or 300 g protein or amino acids/kg feed. The diets were fed for 3 weeks. At the low dietary protein level, whey protein v. casein did not affect plasma total cholesterol, but lowered the concentration of liver cholesterol. At the high dietary protein level, whey protein significantly lowered plasma and liver cholesterol and also plasma triacylglycerols. The hypocholesterolaemic effect of whey protein was associated with a decrease in very-low-density-lipoprotein cholesterol. At the high dietary protein concentration, whey protein reduced the faecal excretion of bile acids when compared with casein. The effects of intact whey protein v. casein were not reproduced by the amino acid mixtures simulating these proteins. It is suggested tentatively that the cholesterol-lowering effect of whey protein in rats is caused by inhibition of hepatic cholesterol synthesis. |
| Lowering high plasma cholesterol levels is not dangerous Schwandt, P., W. O. Richter, et al. (1995), Arch Intern Med 155(9): 985. |
| Lowering increased cholesterol--prolonging life? Klepzig, H., Jr. and M. Kaltenbach (1992), Versicherungsmedizin 44(6): 192-4. Abstract: Epidemiologic surveys reveal a positive correlation between serum cholesterol levels and the incidence of coronary artery disease. Intervention trials demonstrated that a reduction of serum cholesterol by 1% results in a decrease of coronary non-fatal events by 2%. Fatal coronary events remain almost uninfluenced. On the other side, several intervention trials showed an excess mortality from non-cardiac causes in the therapy groups (i.e. malignant tumors, suicides, accidents). Thus, until now no prolongation of life expectancy could be verified by cholesterol lowering measures. |
| Lowering LDL cholesterol: questions from recent meta-analyses and subset analyses of clinical trial DataIssues from the Interdisciplinary Council on Reducing the Risk for Coronary Heart Disease, ninth Council meeting Gotto, A. M., Jr. and S. M. Grundy (1999), Circulation 99(8): E1-7. Abstract: The benefit of cholesterol-lowering therapy in the prevention of coronary heart disease (CHD) is well established. The secondary prevention Scandinavian Simvastatin Survival Study (4S) and the primary prevention West of Scotland Coronary Prevention Study (WOSCOPS) demonstrated that lipid lowering with a statin can dramatically and cost-effectively reduce CHD morbidity and mortality with no increase in noncardiovascular mortality. The Cholesterol and Recurrent Events (CARE) trial extended benefit to CHD patients without high cholesterol. Post hoc analyses of data from these large trials are contributing to speculation, driven by subset analyses and meta-analyses, about whether cholesterol intervention should be target based, as current guidelines recommend. Whereas CARE data support the importance of baseline LDL cholesterol (LDL-C), with greatest clinical event risk reduction in the upper part of the LDL-C range in the trial, 4S found no difference in outcome according to baseline LDL-C in a quartile analysis, and WOSCOPS found no linear relation between decrease in LDL-C and decrease in relative risk for CHD. Furthermore, WOSCOPS showed no additional clinical benefit with LDL-C lowering beyond approximately 24%. Questions raised by such analyses require answers from prospective, hypothesis-based data, and at present there is no compelling argument for moving away from LDL-C targets. The hypothesis-based findings of 4S, CARE, and WOSCOPS support current clinical guidelines, and lowering LDL-C may reduce risk more substantially than might have been predicted. |
| Lowering low density lipoprotein cholesterol with simvastatin, a hydroxy-3-methylglutaryl-coenzyme a reductase inhibitor, does not affect luteal function in premenopausal women Plotkin, D., S. Miller, et al. (2002), J Clin Endocrinol Metab 87(7): 3155-61. Abstract: In this double-blind, randomized, placebo-controlled study, normally cycling women (n = 86) with elevated low density lipoprotein cholesterol (LDL-C) levels were studied over six menstrual cycles. At the end of the screening phase, participants received placebo for the second menstrual cycle and subsequently were randomized to receive either placebo or simvastatin (40 mg/d) for the next four cycles. The second and sixth menstrual cycles were considered baseline and treatment cycles, respectively. Participants kept a menstrual diary throughout the study and provided daily first-void urine samples during cycles 2 and 6. Urine samples were assayed for LH and pregnanediol glucuronide (PdG). The primary end point was change in luteal phase duration as defined by the day of the urinary LH peak to the day preceding the onset of menstruation. Treatment with simvastatin (40 mg/d) effectively lowered LDL-C by 34.3% (P < 0.001). Simvastatin was generally well tolerated, and no meaningful difference in adverse event profile was observed between treatment groups. Compared with the placebo group, simvastatin did not have clinically relevant effects on luteal phase duration, peak PdG concentration, or integrated luteal phase PdG concentration. The results of this study demonstrate that treatment of healthy premenopausal women for approximately 4 months with simvastatin (40 mg/d) lowers LDL-C without adversely affecting reproductive gonadal function. Simvastatin should not be used during pregnancy or by nursing mothers. |
| Lowering low-density cholesterol with diet: the important role of functional foods as adjuncts Stone, N. J. (2001), Coron Artery Dis 12(7): 547-52. |
| Lowering of cholesterol levels and the risk of stroke Davey Smith, G. and S. Ebrahim (1998), Arch Intern Med 158(1): 98-9. |
| Lowering of cholesterol. What role is played by the choice of statins? Marz, W. (2004), MMW Fortschr Med 146(35-36): 55. |
| Lowering of HDL cholesterol in post-menopausal women by tibolone is not associated with changes in cholesterol efflux capacity or paraoxonase activity von Eckardstein, A., K. Schmiddem, et al. (2001), Atherosclerosis 159(2): 433-9. Abstract: Low HDL cholesterol increases the risk of coronary heart disease. Treatment of postmenopausal women with tibolone lowers HDL cholesterol. We elucidated the consequences of this unwanted side effect in a randomized, double-blind study, where 12 women received 2.5 mg tibolone per day and 6 women, placebo. Blood samples were collected on days -1 (i.e. baseline), 28, 56, and 84 for the analysis of various parameters of lipid metabolism and HDL function. Compared to placebo, treatment with tibolone led to statistically significant decreases of HDL cholesterol (-22% to -32%), apoA-I (-14% to -22%), and HDL subclass LpA-I (-30% to -40%) but to no significant changes in apoA-II and HDL subclass LpA-I,A-II. These changes were not associated with statistically significant changes in the activity of plasma to release 3H-cholesterol from radiolabeled fibroblasts or in the serum activity of the anti-oxidative enzyme paraoxonase/arylesterase. There were no significant changes in either serum levels of triglycerides, LDL cholesterol, apoB, and leptin, or in LDL size. We conclude that changes in insulin do not contribute to the lowering of HDL cholesterol by tibolone. Despite decreased HDL cholesterol, putatively anti-atherogenic activities of HDL remained unchanged. |
| Lowering of HDL2-cholesterol and lipoprotein A-I particle levels by increasing the ratio of polyunsaturated to saturated fatty acids Fumeron, F., L. Brigant, et al. (1991), Am J Clin Nutr 53(3): 655-9. Abstract: The protective role of high-density lipoproteins (HDLs) has been attributed to the subfractions HDL2 (according to the density) and lipoprotein A-I (LpA-I) (according to the composition in apolipoproteins). We investigated the effect of a high ratio of polyunsaturated to saturated fatty acids (P:S) on these subfractions in a homogeneous group of young adult males. Two prescribed diets were consumed successively at the subjects' homes for 3 wk each in a random order; one diet contained 70 g butter (P:S 0.2, diet B), the other contained 70 g sunflower margarine (P:S 1.1, diet M). Total calorie, fat, and cholesterol intakes were similar for the two diets. Cholesterol and apolipoprotein B in serum and in low-density lipoproteins (LDLs) were lower with diet M than with diet B. However, significant decreases in protective subfractions of HDL, HDL2, and LpA-I were observed. This undesirable effect of the diet with a high P:S could cancel the benefits of lowering the LDL-cholesterol concentrations. |
| Lowering of LDL cholesterol Payne, N. and C. McCabe (1999), Lancet 354(9185): 1207-8. |
| Lowering of LDL cholesterol Sniderman, A. D. (2000), Lancet 355(9199): 235. |
| Lowering of LDL cholesterol rather than moderate weight loss improves endothelium-dependent vasodilatation in obese women with previous gestational diabetes Bergholm, R., M. Tiikkainen, et al. (2003), Diabetes Care 26(6): 1667-72. Abstract: OBJECTIVE: Effects of weight loss on vascular function are unknown. We compared, in the face of similar weight loss over 3-6 months, effects of orlistat (120 mg t.i.d., n = 23) and placebo (n = 24) on in vivo endothelial function in a high-risk group of obese (BMI 32.1 +/- 0.4 kg/m(2)) premenopausal nondiabetic women with a history of gestational diabetes. RESEARCH DESIGN AND METHODS: Forearm blood flow responses to intra-arterial infusions of acetylcholine (ACh) and sodium nitroprusside (SNP), body composition, and serum lipids were determined before and after weight loss. RESULTS: Weight loss averaged 7.3 +/- 0.2 kg (8.3 +/- 0.1%) and 7.4 +/- 0.2 kg (8.2 +/- 0.1%) of initial body weight in the orlistat and placebo groups, respectively. Forearm and body compositions changed similarly in both groups. Responses to ACh increased by 41% to the low dose (5.9 +/- 0.6 vs. 8.3 +/- 0.3 for flow in the experimental/control arm, P < 0.01) and by 33% to the high dose (7.6 +/- 0.8 vs. 10.1 +/- 0.6, P < 0.001) in the orlistat group, but they remained unchanged in the placebo group. The blood flow responses to SNP did not differ significantly between the groups. LDL cholesterol decreased significantly in the orlistat group from 3.5 +/- 0.2 to 3.0 +/- 0.1 mmol/l (P < 0.01) but remained unchanged in the placebo group. Within the orlistat group, the decrease in LDL cholesterol correlated significantly with the improvement in the blood flow response to ACh (r = -0.44, P < 0.05). CONCLUSIONS: Orlistat but not moderate (8%) weight loss per se improves endothelial function in women with previous gestational diabetes. This improvement is associated with a lowering of LDL cholesterol by orlistat. |
| Lowering of plasma cholesterol levels in animals by lovastatin and simvastatin Chao, Y., J. S. Chen, et al. (1991), Eur J Clin Pharmacol 40 Suppl 1: S11-4. Abstract: Lovastatin and simvastatin are potent competitive inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase. Key inhibit the synthesis of cholesterol in cultured HepG23 cells, rat hepatocytes and in rats. The primary target organ of cholesterol synthesis inhibition by lovastatin and simvastatin is the liver. Lovastating and simvastatin lower levels of plasma cholesterol in rats, dogs and rabbits by inhibition the endogenous cholesterol synthesis and induction of LDL receptor in the liver. |
| Lowering of plasma LDL cholesterol in hamsters by the tomato glycoalkaloid tomatine Friedman, M., T. E. Fitch, et al. (2000), Food Chem Toxicol 38(7): 549-53. Abstract: Tomatoes contain the steroidal glycoalkaloid tomatine, which has been reported to form strong, insoluble complexes with cholesterol in vitro. To determine whether tomatine can reduce dietary cholesterol absorption and plasma levels of cholesterol and triglycerides, we fed hamsters a high-fat, high-cholesterol diet with 0.05-0.2% added tomatine in the diet. The tomatine diets induced lowering of serum low-density lipoprotein (LDL) without changing high-density lipoprotein (HDL) cholesterol. Compared to the control diets, four- to fivefold more labeled dietary cholesterol and coprostanol was excreted in the feces of the tomatine-fed hamsters. The amount of cholesterol excreted in the feces corresponded to the amount of tomatine in the diet. These observations suggest that due to the formation of an insoluble tomatine-cholesterol complex and its excretion in the feces, very little dietary tomatine is absorbed from the digestive tract into the blood stream. They are also consistent with the reported low oral toxicity of tomatine compared to other glycoalkaloids. |