Cholesterol Journal Articles

Record 7981 to 8000

Iron and zinc status of women and men who followed cholesterol-lowering diets
Retzlaff, B. M., B. L. Buck, et al. (1998), J Am Diet Assoc 98(2): 149-54.
Abstract: OBJECTIVE: To determine if men and women taught the National Cholesterol Education Program step 2 diet experienced diminished iron or zinc status after 2 years of consuming the diet. DESIGN: Subjects attended 8 weeks of diet classes and followup counseling. Four-day food records, zinc protoporphyrin/ heme (ZPP/H, a measure of iron stores), hematocrit, and plasma zinc values were collected at baseline, 1 year, and 2 years. SUBJECTS: Participants in a study of the efficacy of the step 2 diet (213 men and 151 women) who had low-density lipoprotein cholesterol levels above the 75th percentile, and who were not taking lipid-altering medication. STATISTICAL ANALYSES: Paired t tests to compare preintervention and postintervention test results. Two-sample t tests to compare gender, menopause status, and hormone-use groups. Analysis of variance was performed to compare plasma zinc levels among diet-adherence subgroups. Individual evaluation of outlying values and backward stepwise regression to determine the independent effects of variables were also completed. RESULTS: Mean dietary intake approached or exceeded step 2 guidelines. Density of iron intake increased. Density of zinc intake was unchanged, but mean intake was low. Mean ZPP/H and hematocrit did not change for premenopausal or postmenopausal women with or without supplemental hormones; men's values changed only slightly. Abnormal ZPP/H and hematocrit occurred sporadically. Mean plasma zinc levels did not differ from baseline for women, increased slightly for men, and did not differ by level of dietary adherence. No plasma zinc concentrations were below normal. APPLICATION: In this large-scale, 2-year prospective study of women and men, no adverse effects on intake or plasma indicators of iron and zinc were detected as a result of subjects being taught the NCEP step 2 diet.

Iron deficiency enhances cholesterol gallstone formation
Johnston, S. M., K. P. Murray, et al. (1997), Surgery 122(2): 354-61; discussion 361-2.
Abstract: BACKGROUND: Cholesterol gallstones occur most commonly in multiparous women, but the causes for this phenomenon remain unclear. This same patient population is prone to chronic iron deficiency anemia. In addition, iron is known to play an important role in hepatic enzyme metabolism. Therefore, we tested the hypotheses that iron deficiency would alter hepatic cholesterol metabolism and enhance gallstone formation. METHODS: Forty adult prairie dogs were fed either a control iron-supplemented (200 ppm), an iron-deficient (8 ppm), a 0.4% cholesterol iron-supplemented (200 ppm), or a 0.4% cholesterol iron-deficient (8 ppm) diet. After 8 weeks gallbladder bile, serum, and liver were harvested. Gallbladder bile was examined for cholesterol crystals and gallstones. Bile lipids and hepatic enzymes were measured, and a cholesterol saturation index (CSI) was calculated. RESULTS: Animals receiving the iron-deficient diet were more likely to have cholesterol crystals in their bile than were animals on the control diet (80% vs. 20%; p < 0.05). Animals on the 0.4% cholesterol iron-deficient diet had more cholesterol crystals per high-powered field (79 +/- 10 vs. 49 +/- 9; p = 0.07), a higher molar % cholesterol (6.0 +/- 0.3 vs 4.4 +/- 0.5; p < 0.05), and a higher CSI (1.27 +/- 0.10 vs. 0.91 +/- 0.07; p < 0.05) compared to animals receiving the 0.4% cholesterol iron supplemented diet. The 7 alpha-hydroxylase levels were lower in the animals on the iron-deficient diet compared to those receiving the control diet (0.42 +/- 0.08 vs 1.17 +/- 0.40 pmol/mg per minute; p = 0.07). CONCLUSIONS: These data suggest that an iron-deficient diet (1) alters hepatic enzyme metabolism, which, in turn, (2) increases gallbladder bile cholesterol and promotes cholesterol crystal formation. We conclude that iron deficiency plays a previously unrecognized role in the pathogenesis of cholesterol gallstone formation in women.

Iron loading increases cholesterol accumulation and macrophage scavenger receptor I expression in THP-1 mononuclear phagocytes
Kraml, P. J., R. L. Klein, et al. (2005), Metabolism 54(4): 453-9.
Abstract: Epidemiological studies have established that a high level of iron body stores is associated with increased risk of acute coronary heart disease. To explain this association, it has been proposed that iron catalyzes the production of highly reactive forms of free oxygen species, and thus, promotes low-density lipoprotein (LDL) oxidation, a lipoprotein that plays a critical role in atherogenesis. However, few studies have provided evidence to support this hypothesis. In the present study, we determined the effect of iron loading of THP-1 mononuclear phagocytes on LDL metabolism. We demonstrated that iron loading of THP-1 cells stimulated conjugated diene formation in LDL in the culture medium. In addition, iron loading of THP-1 cells significantly increased cholesteryl ester accumulation in cells exposed to native LDL, suggesting that during the incubation of the cells with native LDL, the LDL became oxidized and was taken up by the cells. We further demonstrated that the degradation of 125I-oxidized LDL was significantly increased in iron-loaded THP-1 cells. Lastly, we demonstrated that iron loading of THP-1 cells stimulated scavenger receptor expression in these cells. In conclusion, this study demonstrates that loading of mononuclear phagocytes with iron leads to oxidization of LDL, increased cellular cholesterol accumulation and scavenger receptor expression, and supports the hypothesis that increased macrophage iron levels promote atherogenesis.

Iron versus cholesterol--perspectives on the iron and heart disease debate
Sullivan, J. L. (1996), J Clin Epidemiol 49(12): 1345-52.
Abstract: Focusing only on the limited question of whether stored iron is a valid heart disease risk factor inappropriately narrows the scope of the debate on the "iron hypothesis." Framing the debate in this way ignores the broad explanatory power of the hypothesis that iron depletion protects against ischemic heart disease. The iron hypothesis provides a conceptual tool for study of the mechanisms by which age and gender influence the development of ischemic heart disease. The assumption that age and gender exert unalterable effects has diverted attention from these strong risk factors, and has led to intense preoccupation with weaker risk factors such as cholesterol. The notion that cholesterol is of central importance has become a rigid and institutionalized point of view. Increased mortality from some cholesterol-lowering drugs is but one of the potential dangers of continued promotion of the flawed idea that heart disease is a function of the cholesterol concentration. The more serious risk is that alternative approaches to the problem of ischemic heart disease will be suppressed. Consideration of the relationship between the iron and cholesterol hypotheses provides important perspectives on the current debate on the role of iron in the development of ischemic heart disease.

Iron versus cholesterol--response to dissent by Weintraub et al
Sullivan, J. L. (1996), J Clin Epidemiol 49(12): 1359-62.

Iron worsens high-cholesterol-related coronary artery disease
Herbert, V. (1994), Am J Clin Nutr 60(2): 299-300.

Iron, atherosclerosis, and neurodegeneration: a key role for cholesterol in promoting iron-dependent oxidative damage?
Ong, W. Y. and B. Halliwell (2004), Ann N Y Acad Sci 1012: 51-64.
Abstract: This article reviews the roles and interactions of iron, atherosclerosis, and neurodegeneration. It highlights the importance of cholesterol in promoting iron-dependent oxidative damage. An intriguing possibility is that hypercholesterolemia can increase brain iron load and both the aggregation of beta-amyloid and the ability of iron on plaques to catalyze oxidative damage. This could explain why hypercholesterolemia is a risk factor for Alzheimer's disease. Further work is necessary to study the mechanism of increased iron transport across the blood brain barrier in atherosclerosis.

Is a high serum cholesterol level associated with longer survival in elderly hypertensives?
Staessen, J., A. Amery, et al. (1990), J Hypertens 8(8): 755-61.
Abstract: The relationship between serum total cholesterol, measured at randomization, and mortality was investigated in 822 patients, who were followed for an average of 3.1 years in a double-blind trial, conducted by the European Working Party on High Blood Pressure in the Elderly. Serum cholesterol, measured at randomization, was 0.54 mmol/l higher in women than in men, and declined with increasing age in both men (0.028 mmol/l per year) and women (0.036 mmol/l per year). During follow-up on randomized treatment, cholesterol fell by a similar amount with placebo (0.11 mmol/l per year) and with active treatment (0.14 mmol/l per year). Active treatment consisted of hydrochlorothiazide (25-50 mg/day) plus triamterene (50-100 mg/day) with the addition of alpha-methyldopa (0.5-2.0 g/day) in one-third of the patients. Serum total cholesterol, measured at randomization, was independently and inversely correlated with total (P = 0.03), non-cardiovascular (P = 0.03) and cancer (P = 0.04) mortality during follow-up on double-blind treatment. Total and non-cardiovascular mortality were also negatively correlated with haemoglobin and body weight at randomization.

Is a low fat diet enough to achieve serum cholesterol goals?
Eichholzer, M. and F. Gutzwiller (1999), Eur Heart J 20(14): 991-4.

Is a role of phospholipase A(2) in cholesterol gallstone formation phospholipid species-dependent?
Sunami, Y., S. Tazuma, et al. (2001), Biochim Biophys Acta 1532(1-2): 51-9.
Abstract: Phospholipase A(2) plays a role in cholesterol gallstone formation by hydrolyzing bile phospholipids into lysolecithin and free fatty acids. This study investigated its effects on cholesterol crystallization in model bile systems. Supersaturated model bile solutions with different cholesterol saturation indexes (1.2, 1.4, and 1.6) were prepared using cholesterol, taurocholate, and egg yolk phosphatidylcholine, soybean phosphatidylcholine, palmitoyl-oleoyl phosphatidylcholine, or palmitoyl-linoleoyl phosphatidylcholine. Then the effect of digestion of phosphatidylcholine by phospholipase A(2) on bile metastability was assessed by spectrophotometry and video-enhanced differential contrast microscopy. Addition of phospholipase A(2) caused the release of free fatty acids in a time-dependent manner. Cholesterol crystallization was enhanced by an increased crystal growth rate in model bile containing hydrophilic species such as soybean or palmitoyl-linoleoyl phosphatidylcholine, consisting predominantly of polyunsaturated fatty acids. Because phospholipase A(2) enhanced cholesterol crystallization in bile containing hydrophilic phosphatidylcholine species, but not hydrophobic phosphatidylcholine species, release of polyunsaturated fatty acids by hydrolysis may be responsible for such enhancement. Therefore, the role of phospholipase A(2) in cholesterol gallstone formation depends on the phospholipid species present in bile, so that phospholipid species selection during hepatic excretion is, in part, crucial to the cholesterol stone formation.

Is abnormal postprandial lipemia a familial risk factor for coronary artery disease in individuals with normal fasting concentrations of triglycerides and cholesterol?
Przybycien, K., Z. Kornacewicz-Jach, et al. (2000), Coron Artery Dis 11(5): 377-81.
Abstract: OBJECTIVE: To assess the postprandial response to a fat load in patients with coronary artery disease (CAD) and age-matched controls. METHODS: Postprandial lipemia was assessed in patients with CAD confirmed by angiography (study group, n = 44) and in patients without coronary lesions (control group, n = 20). Family members of patients with CAD were also included (spouses group, n = 22; progeny group, n = 33). Fasting triglyceride and cholesterol concentrations in the control and study groups were less than 2.3 and 6.47 mmol/l, respectively. After initial blood sampling, the patients consumed 30% cream (200 ml/m2 body area). Repeat measurements of triglycerides, total cholesterol and high-density lipoprotein were made after 2, 4, 6, and 8 h. RESULTS: Changes were most marked in triglyceride concentrations. Peak values were observed after 4 h in the spouses, progeny, and control groups, and after 6 h in the study group. To compensate for the large age span (8-40 years) of the progeny, two subgroups were formed, taking 25 years as the cut-off value. Triglycerides continued to increase until the 4th hour in both subgroups, but the subgroups differed as to the absolute concentration of triglycerides. During the first 6 h of the test, the concentrations were significantly greater in the subgroup of older progeny than in their fathers with CAD. CONCLUSIONS: These findings indicate that triglycerides are metabolized at a slower rate and remain longer in the circulation of patients with CAD, as compared with patients without CAD. A significantly greater level of postprandial lipemia has been observed in adult progeny of patients with CAD, suggesting a genetic disorder of triglyceride metabolism in these individuals.

Is aggressive cholesterol control justified? Review of the post-coronary artery bypass graft trial
Hunninghake, D. B. (1998), Am J Cardiol 82(10B): 45T-48T.
Abstract: The Post-Coronary Artery Bypass Graft (CABG) trial was undertaken to compare the efficacy of aggressive low-density-lipoprotein (LDL) cholesterol lowering (<85 mg/dL) with moderate LDL-cholesterol lowering (130-140 mg/dL) in preventing atherosclerotic progression in saphenous vein grafts. In both the aggressive- and moderate-treatment groups, clinicians titrated lovastatin dosages based on individual patients' LDL-cholesterol levels. Based on angiography performed 4-5 years after enrollment, the rate of disease progression was 31% lower in aggressive-treatment patients than in those who received moderate treatment. Compliance with lovastatin therapy was 85-90%. The results confirm that LDL-cholesterol levels should be decreased to <100 mg/dL in patients with coronary artery disease. The challenge is to ensure that at-risk patients receive drug therapy in adequate, individualized doses.

Is atherosclerosis caused by high cholesterol?
Ravnskov, U. (2002), Qjm 95(6): 397-403.

Is atherosclerosis equivalent to cholesterol?
Adeva Andany, M. (1995), Nephron 71(4): 487-8.

Is atherosclerosis in diabetes and impaired fasting glucose driven by elevated LDL cholesterol or by decreased HDL cholesterol?
Drexel, H., S. Aczel, et al. (2005), Diabetes Care 28(1): 101-7.
Abstract: OBJECTIVE: To evaluate the atherogenicity of lipids in coronary patients with normal fasting glucose (NFG), impaired fasting glucose (IFG), and type 2 diabetes. RESEARCH DESIGN AND METHODS: Serum lipid values, the presence of angiographic coronary artery disease (CAD) at baseline, and the incidence of vascular events over 2.3 years were recorded in 750 consecutive patients undergoing coronary angiography. RESULTS: Triglycerides significantly (P < 0.001) increased and HDL cholesterol (P < 0.001) as well as LDL particle diameter (P < 0.001) significantly decreased from subjects with NFG <5.6 mmol/l (n = 272) over patients with IFG > or =5.6 mmol/l (n = 314) to patients with type 2 diabetes (n = 164). Factor analysis revealed two factors in the lipid profiles of our patients: triglycerides, HDL cholesterol, apolipoprotein A1, and LDL particle diameter loaded high on an HDL-related factor, and total cholesterol, LDL cholesterol, and apolipoprotein B loaded high on an LDL-related factor. In patients with type 2 diabetes, the HDL-related factor (odds ratio 0.648 95% CI 0.464-0.904; P = 0.011), but not the LDL-related factor (0.921 0.677-1.251; P = 0.597), was associated with significant coronary stenoses > or =50%. Consistently, in the prospective study, the HDL-related factor (0.708 0.506-0.990; P = 0.044), but not the LDL-related factor (1.362 0.985-1.883; P = 0.061), proved significantly predictive for vascular events in patients with type 2 diabetes. CONCLUSIONS: The low HDL cholesterol/high triglyceride pattern is associated with the degree of hyperglycemia. In coronary patients with type 2 diabetes, this pattern correlates with the prevalence of CAD and significantly predicts the incidence of vascular events.

Is atherosclerosis in diabetes and impaired fasting glucose driven by elevated ldl cholesterol or by decreased hdl cholesterol? response to Drexel et al
Schulze, M. B. and K. Hoffmann (2005), Diabetes Care 28(5): 1264; author reply 1264-5.

Is cholesterol a conditionally essential nutrient in critically ill patients?
Druml, W. (2003), Wien Klin Wochenschr 115(21-22): 740-2.

Is cholesterol a risk factor for stroke? No
Landau, W. M. (1999), Arch Neurol 56(12): 1521-4.

Is cholesterol a risk factor for stroke? Yes
Demchuk, A. M., D. C. Hess, et al. (1999), Arch Neurol 56(12): 1518-20; discussion 1524.

Is cholesterol lowering an alternative to revascularization in some patients with coronary artery disease?
Havranek, E. P. (1995), Arch Intern Med 155(7): 670-6.
Abstract: Cholesterol lowering has been shown to decrease the dimensions of atherosclerotic plaques in some patients with coronary artery disease. Because of this observation, there is growing discussion about whether or not cholesterol lowering might be used in place of revascularization. The available data suggest that cholesterol lowering in place of revascularization may be appropriate for patients with chronic stable angina, for patients who are asymptomatic but have provocable ischemia after myocardial infarction, and for patients at moderate risk for cardiac events as judged by exercise test or clinical variables. The available data do not justify changing current practices; further study is necessary.

Cholesterol Articles and Abstracts

Cholesterol Journal Articles