| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Does bilirubin play a role in the pathogenesis of both cholesterol and pigment gallstone formation? Direct and indirect influences of bilirubin on bile lithogenicity Nakai, K., S. Tazuma, et al. (2001), Biochim Biophys Acta 1534(2-3): 78-84. Abstract: Bilirubin is found in the center of cholesterol gallstones, but its pathogenic role in their formation is unknown. Bilirubin causes a disproportionate reduction of biliary lipid secretion without affecting bile salt secretion in association with a change of biliary lecithin species, which modulates the cholesterol crystallization process. Therefore, the present study investigated whether bilirubin can influence the cholesterol crystallization procedure, and the mechanism(s) of any such action. Supersaturated model bile was prepared (taurocholate/lecithin/cholesterol at 71:18:11, a total lipid concentration of 9.0 g/dl, and cholesterol saturation index of 1.8), and cholesterol crystallization was monitored over time using a spectrophotometer and video-enhanced differential contrast microscopy in the absence or presence of bilirubin (at a final concentration of 10 microM, 20 microM, 40 microM, and 100 microM). Bilirubin enhanced the onset of cholesterol crystallization by 50%, whereas the crystal growth rate and final crystal mass were reduced at a high concentration of bilirubin. Taken together, these results suggest that bilirubin influences the cholesterol crystallization process, by either a direct interaction with biliary lipids that alters metastability, an indirect alteration of the bile salt-micellar lipid holding capacity, or both. Thus, bilirubin may play a role in the pathogenesis of both cholesterol and pigment gallstones. |
| Does body fatness modify the association between dietary cholesterol and risk of coronary death? Results from the Chicago Western Electric Study Goff, D. C., Jr., R. B. Shekelle, et al. (1992), Arterioscler Thromb 12(7): 755-61. Abstract: The hypothesis that body fatness modifies the relation between dietary cholesterol and 25-year coronary mortality was examined in a cohort of 1,792 middle-aged men employed by the Western Electric Company in Chicago. Relative risks of coronary death (and 95% confidence intervals) associated with a 225 mg/day greater intake of dietary cholesterol for men with a subscapular skinfold thickness less than or equal to 14, 15-20, and greater than or equal to 21 mm were 1.44 (1.10-1.90), 1.07 (0.84-1.36), and 0.95 (0.76-1.20), respectively, after adjustment for age; serum total cholesterol level; systolic blood pressure; cigarette smoking; family history of cardiovascular disease; evidence of major organ system disease at baseline; and intake of saturated fatty acids, polyunsaturated fatty acids, energy, and ethanol. Adjusted relative risks associated with a 15-mm greater subscapular skinfold thickness for men with a dietary cholesterol intake less than or equal to 649, 650-799, and greater than or equal to 800 mg/day were 1.76 (1.04-2.98), 1.64 (1.04-2.57), and 1.00 (0.69-1.55), respectively. Fatter men apparently did not benefit from a diet lower in cholesterol, while men who ate a diet high in cholesterol apparently did not benefit from leanness. These results support the hypothesis that body fatness modifies the relation between dietary cholesterol and coronary mortality, perhaps because leaner men are more responsive than fatter men to the effects of dietary cholesterol on the concentration of low density lipoprotein cholesterol. |
| Does body fatness modify the effect of dietary cholesterol on serum cholesterol? Results from the Chicago Western Electric Study Goff, D. C., Jr., R. B. Shekelle, et al. (1993), Am J Epidemiol 137(2): 171-7. Abstract: The hypothesis that lean persons are more responsive than fat persons to the effects of dietary cholesterol was investigated in 1,903 middle-aged employed men who were examined in 1958 and 1959 as participants in the Chicago Western Electric Study. Change in intake of dietary cholesterol was positively associated with change in serum cholesterol for men in the lowest tertile of body mass index (defined as weight (kg)/height (m)2) (< 24.2) but not for men in the highest tertile (> 26.6) after adjustment for change in body mass index and change in intakes of energy and saturated and polyunsaturated fatty acids. A decrease of 150 mg/1,000 kcal in dietary cholesterol was associated with mean changes of -0.46, -0.18, and 0.13 mmol/liter in serum cholesterol for men with body mass indices of < 24.2, 24.2-26.6, and > 26.6, respectively. Body mass index was strongly correlated with subscapular skinfold thickness; thus, these differences in body mass index reflect true differences in adiposity. These results may help to explain inconsistencies that have occurred in feeding experiments with dietary cholesterol, and they suggest that a reduction in dietary cholesterol should have a more favorable effect on the serum cholesterol levels of fat persons after they have lost weight. |
| Does change in serum cholesterol of a population influence coronary heart disease mortality? Sans, S. (1997), Eur Heart J 18(4): 540-3. |
| Does cholesterol depletion have adverse effects on blood rheology? Fawcett, J. P. and D. B. Menkes (1994), Angiology 45(3): 199-206. Abstract: Blood viscosity (eta B) at shear rates 10 and 100s-1, plasma viscosity (eta P), hematocrit (Hct), and whole blood cholesterol (Chol) were measured in 50 patients with a history of myocardial infarction or unstable angina pectoris. Erythrocyte morphology was also studied by scanning electron microscopy to determine the proportion of nondiscocytic erythrocytes (NDE). There was a significant positive correlation between Chol and eta P (r = 0.41, P < 0.004) and a highly significant negative correlation (r = -0.69, P < 0.001) between Chol and Tk, a viscometric index of erythrocyte rigidity based on relative blood viscosity at high shear (eta B/eta P) corrected for Hct. This latter result indicates Chol reduction in this population may increase erythrocyte rigidity. Twenty-five patients with Chol values in the range 4.0-8.0 mmol/L were commenced on a standard lipid-lowering diet and after eight weeks half were also given pravastatin (40 mg daily). After thirty-two weeks Chol had fallen significantly more in the pravastatin group (28%) than in the diet only group (11%, P = 0.005). There was no change in eta P for either group but a significant increase in Tk for the pravastatin group only (P = 0.011). The change in total cholesterol (delta Chol) for each patient over thirty-two weeks was negatively correlated with both the change in the index of erythrocyte rigidity (delta Tk) (r = -0.40, P = 0.044) and the change in the proportion of nondiscocytic erythrocytes (delta NDE) (r = -0.47, P = 0.026). These data suggest that cholesterol reduction within the normolipemic range may be associated with unfavorable changes in blood rheology. |
| Does cholesterol discriminate between sphingomyelin and phosphatidylcholine in mixed monolayers containing both phospholipids? Mattjus, P. and J. P. Slotte (1996), Chem Phys Lipids 81(1): 69-80. Abstract: The objective of this work was to examine the interaction of cholesterol with both phosphatidylcholines, 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC) or 1,2-dipalmitoyl-sn-glycero-3-phosphocholine (DPPC), and sphingomyelins, N-oleoyl-D-sphingomyelin (O-SPM) or N-palmitoyl-D-sphingomyelin (P-SPM), in monolayers at an air/water interface. We used cholesterol oxidase to probe for the relative strength of sterol-phospholipid interaction, and fluorescence microscopy to visualize lateral domain formation in the mixed monolayers. The ternary mixed monolayers, which contained cholesterol, POPC, and O-SPM had a twofold higher average oxidation rate than the corresponding system containing DPPC and P-SPM. This difference in oxidation rate between saturated and unsaturated systems was observed irrespective of the ratio between phosphatidylcholine and sphingomyelin in the monolayer. With either the saturated or the unsaturated systems, however, the rate of oxidation was influenced by the ratio of phosphatidylcholine to sphingomyelin. As the monolayer content of phosphatidylcholine increased and the sphingomyelin content decreased correspondingly (to maintain a constant cholesterol-to-phospholipid molar ratio), an increase in the average oxidation rate was seen in both saturated and mono-unsaturated monolayer systems. The relationship between the rate of cholesterol oxidation and the phosphatidylcholine/sphingomyelin ratio was not linear, suggesting a preferential interaction of cholesterol with sphingomyelin even when phosphatidylcholine was present in the monolayer. The formation and stability of cholesterol-rich lateral (liquid-condensed) domains in the monolayers, as determined by monolayer fluorescence microscopy, was found to be highly influenced by the phospholipid class, the degree of acyl chain saturation, and by the ratio of phosphatidylcholine to sphingomyelin in the monolayer. The differences in cholesterol oxidation rates and lateral domain formation, as a function of the ratio of two phospholipids in the monolayers, apparently derived from differences in the hydrophobic interactions between the lipids. |
| Does cholesterol lowering increase non-illness-related mortality? Muldoon, M. F., S. B. Manuck, et al. (1991), Arch Intern Med 151(7): 1453-4. |
| Does cholesterol screening result in negative labeling effects? Results of the Massachusetts Model Systems for Blood Cholesterol Screening Project Havas, S., J. Reisman, et al. (1991), Arch Intern Med 151(1): 113-9. Abstract: Several previous studies that looked at the effects of labeling individuals as hypertensive found increases in psychosocial distress, diminished feelings of well-being, or absenteeism. Other studies found no such effects. Thus far, similar studies relating to labeling for high blood cholesterol levels have not been published. The Massachusetts Model Systems for Blood Cholesterol Screening Project investigated whether labeling effects occurred as a result of the community-based screening, education, and referral programs it conducted in Worcester and Lowell. Nine questions concerning perceptions of physical and psychological well-being were asked on a questionnaire given to screening participants. The same questions were asked as part of a follow-up questionnaire given to all individuals identified as having high blood cholesterol levels at one of the screenings. Comparison of the baseline and follow-up results did not demonstrate significant overall negative effects among any age, sex, racial, income, or educational groups. On the contrary, responses to many of the questions revealed small but statistically significant improvements in perceptions of physical and psychological well-being. The absence of negative labeling effects may be attributable to the positive, supportive approach to participant counseling taken by the project. |
| Does cholesterol use the mitochondrial contact site as a conduit to the steroidogenic pathway? Thomson, M. (2003), Bioessays 25(3): 252-8. Abstract: The first and rate-limiting step of steroidogenesis is the transfer of cholesterol from the outer mitochondrial membrane to the inner membrane where it is converted to pregnenolone by cytochrome P450 side-chain cleavage (P450scc). This reaction is modulated in the gonads and adrenals by the steroidogenic acute regulatory protein (StAR), however, the mechanism used by StAR is not understood. The outer and inner mitochondrial membranes are joined at contact sites that are thought to be held in place by protein complexes that bridge the two membranes. While it is generally accepted that proteins are imported into the mitochondrion via contact sites, it is not clear whether cholesterol takes the same conduit to the inner membrane. Strategies to combat diseases caused by interrupted cholesterol transfer will rely on a full understanding of the steroidogenic mechanism. The challenge for the future is to determine whether StAR relies on the molecular architecture that spans the mitochondrial intermembrane space to deliver its cargo. |
| Does enolase have a role in cholesterol metabolism? Shand, J. H. and D. W. West (1994), Biochem Soc Trans 22(4): 435S. |
| Does exercise increase HDL cholesterol in those who need it the most? Thompson, P. D. and D. J. Rader (2001), Arterioscler Thromb Vasc Biol 21(7): 1097-8. |
| Does fat in milk, butter and cheese affect blood lipids and cholesterol differently? Tholstrup, T., C. E. Hoy, et al. (2004), J Am Coll Nutr 23(2): 169-76. Abstract: OBJECTIVE: To compare the effects of isoenergetic amounts of milk, cheese and butter (adjusted to the same content of lactose and casein) on fasting and postprandial blood lipids and lipoproteins, and on postprandial glucose and insulin response. DESIGN: The experiments were designed to provide 20% of total energy from dairy fat, as either whole milk, mean (+/-SD) 2164 (+/-97) g, butter 93 (+/-4) g, and hard cheese 305 (+/-45) g, which were served to 14 healthy young men for three periods of three weeks each, separated by washout periods, in a randomized, cross-over study with strictly controlled dietary intake. Fasting blood samples were taken at the end of the study periods. Measurements of the postprandial effect of the three different dairy test products (0.7 g of milk fat/kg body weight) were carried out on day 4 of each intervention period. Blood samples were taken before and at 2, 4, 6 and 8 hours following intake of the meals. RESULTS: Fasting LDL cholesterol concentration was significantly higher after butter than cheese diet (p = 0.037), with a borderline significant difference in total cholesterol (p = 0.054) after the experimental periods of three weeks. Postprandial glucose showed a higher response after cheese diet than after milk diet (p = 0.010, diet x time interaction). CONCLUSIONS: A different effect of fat in milk and butter could not be confirmed in this study. The moderately lower LDL cholesterol after cheese diet compared to butter diet should be investigated further. |
| Does increased crypt cell proliferation impair cholesterol absorption after proximal gut resection? Pakarinen, M. P., T. A. Miettinen, et al. (2000), Scand J Gastroenterol 35(7): 719-25. Abstract: BACKGROUND: The effects of proximal small-bowel resection on absorption and synthesis of cholesterol are unclear. METHODS: To study cholesterol absorption and synthesis after proximal gut resections of variable length, plasma plant sterols, cholestanol, and cholesterol precursors were measured 1 and 2 months after 50% and 75% proximal small-bowel resection or transection. To examine the effect of increased crypt cell proliferation and brush border development on cholesterol absorption, the results were related to the mucosal morphology, crypt cell proliferation, and disaccharidase activities of the remaining small bowel. RESULTS: Campesterol levels in proportion to cholesterol decreased markedly more, and those of cholestanol markedly less, than would be expected simply due to the amount of proximal small intestine removed, whereas sitosterol proportions decreased in proportion to the length of gut resection. Campesterol proportions markedly (P = 0.06) increased between 1 and 2 months after 50% resection but remained unchanged after 75% resection. Crypt cell proliferation was only increased in the 75% resection group (P < 0.05). The longer the proximal gut resection, the lower was the mucosal enzyme activity. Both resection groups showed increased plasma cholesterol precursor proportions and crypt depth (P < 0.05), whereas villus height remained unchanged. After massive proximal resection campesterol and sitosterol proportions were inversely related to crypt cell proliferation (r = -0.86-0.83, P < 0.01). CONCLUSIONS: Increased crypt cell proliferation activated by massive proximal gut resection may act as a previously unrecognized factor in aggravating cholesterol malabsorption and retarding its recovery during the early postoperative period. These findings warrant further investigation. |
| Does industrial environment influence the prevalence of arterial hypertension, plasma cholesterol and uric acid concentration and activity of the renin-aldosterone system? Wiecek, A. and F. Kokot (1996), Przegl Lek 53(4): 356-9. Abstract: The present study aimed to assess the influence of a highly industrialized environment on the prevalence of arterial hypertension and plasma levels of cholesterol, uric acid, aldosterone and plasma renin activity. Epidemiological studies were performed in 5008 inhabitants of a highly industrialized city (Piekary Slaskie) and in 5004 inhabitants of non industrialized city (Olesno Slaskie) in the south part of Poland. Only subjects over 15 years were enrolled. The prevalence of arterial hypertension in the industrial population was 17% while in the country city 8.2%. Significantly higher serum cholesterol levels were found in hypertensive and normotensive subjects of the highly industrialized region than in the non industrialized one. Finally in hypertensive women aged < 40 years and normotensive men and women of the industrialized region significantly higher plasma renin activity and plasma aldosterone concentration were found than in corresponding population groups of the non industrialized region. From the results obtained in this study it seems, that the highly industrialized environment seems to stimulate hypertensinogenic factors. |
| Does inflammation or undernutrition explain the low cholesterol-mortality association in high-functioning older persons? MacArthur studies of successful aging Hu, P., T. E. Seeman, et al. (2003), J Am Geriatr Soc 51(1): 80-4. Abstract: OBJECTIVES: To explore the effect of inflammation and undernutrition on the association between hypocholesterolemia and higher overall mortality in high-functioning older persons. DESIGN: Prospective cohort study. SETTING: Three U.S. communities. PARTICIPANTS: A cohort of 870 participants from the MacArthur Studies of Successful Aging. MEASUREMENTS: Baseline information was obtained for serum levels of cholesterol, C-reactive protein, interleukin-6, and albumin; body mass index; prevalent medical conditions; health behaviors; and medications. Crude and multivariate logistic regression analyses were used to examine the association between serum total cholesterol levels and 7-year all-cause mortality, while adjusting for potential confounders. RESULTS: In univariate analysis, the risk ratio of low serum total cholesterol level (<169 mg/dL) for 7-year total mortality was 1.90 (95% confidence interval (CI) = 1.18-3.07). The multiple adjusted risk ratios were 1.82 (95% CI = 1.10-3.00) after controlling for markers of inflammation and nutrition and 1.39 (95% CI = 0.80-2.40) after adjustment for additional cardiovascular risk factors. Sex was an important confounding variable that contributed to the observed inverse association between low serum cholesterol and overall mortality in univariate analysis. CONCLUSIONS: Hypocholesterolemia is not an independent risk factor for increased overall mortality in high-functioning community-dwelling older men and women. The association between low total cholesterol and high mortality observed in crude analysis is mainly confounded by common cardiovascular risk factors, rather than underlying inflammation or undernutrition. |
| Does low cholesterol cause death? Rossouw, J. E. and A. M. Gotto, Jr. (1993), Cardiovasc Drugs Ther 7(5): 789-93. Abstract: Data linking low cholesterol with excess mortality have been gathered from both observational and clinical trials. The data are probably unrelated, as the levels of total cholesterol associated with excess mortality in observational studies are well below 160 mg/dl (4.1 mmol/l), whereas the levels achieved in clinical trials average around 230 mg/dl (5.9 mmol/l). Likely explanations of the association are that low cholesterol is a consequence of disease or is a confounder associated with other variables. The authors assess the relevance of the data to public health policy and medical practice. They conclude that evidence suggesting low cholesterol is a cause of excess mortality currently lacks breadth and rigor, and find no basis for changing cholesterol-management guidelines. |
| Does lowering of cholesterol levels influence functional properties of large arteries? Kool, M., F. Lustermans, et al. (1995), Eur J Clin Pharmacol 48(3-4): 217-23. Abstract: Hypercholesterolaemia is a risk factor for atherosclerosis and induces endothelial dysfunction. Endothelial dysfunction may increase vascular tone and arterial stiffness and as a consequence may decrease arterial distensibility (DC) and arterial compliance (CC). It is hypothesized that lipid-lowering therapy may enhance DC and CC. Therefore, the present study investigates the effect of lipid-lowering therapy with pravastatin on the haemodynamics, DC and CC of the elastic common carotid artery (CCA), and the muscular femoral (FA) and brachial (BA) arteries in patients with primary hypercholesterolaemia. After an 8-week placebo run-in period with a low-cholesterol diet, 19 patients with total cholesterol concentrations of between 6.5 and 9.0 mmol.l-1 and triglyceride concentrations < 4 mmol.l-1 entered a double-blind placebo controlled crossover study. Patients received pravastatin 40 mg o.d. or placebo, each for 8 weeks. Throughout the study the lipid-lowering diet was continued. With pravastatin, total cholesterol, low-density lipoprotein cholesterol (LDL-C) and triglycerides were decreased (total cholesterol 26%, LDL-C 35%, triglycerides 16%), while high-density lipoprotein cholesterol (HDL-C) was not changed. Other laboratory values remained within the normal range. Blood pressure, heart rate, cardiac function and systemic vascular resistance were not influenced by pravastatin. Compared to placebo, diameter, distensibility and compliance of all arteries were not statistically significantly changed with pravastatin. These data suggest that, in patients with mild to moderate primary hypercholesterolaemia, short-term lowering of plasma cholesterol does not alter the haemodynamics and vessel wall properties of large arteries. |
| Does lowering serum cholesterol levels lower coronary heart disease risk? Rossouw, J. E. and B. M. Rifkind (1990), Endocrinol Metab Clin North Am 19(2): 279-97. Abstract: Many lines of evidence converge toward the conclusion that low-density lipoprotein cholesterol (LDLC) is indeed a causal factor in the genesis of CHD. These range from animal studies, pathology studies, inborn errors of metabolism, clinical observations, and the existence of plausible biologic mechanisms, to the vast body of epidemiologic evidence. Observations of the association of LDLC with CHD hold between different populations, in the same population at different times, and to studies of individuals within populations. Finally, the clinical trials of cholesterol lowering, together with regression studies in animals and angiographic studies in humans, provide compelling evidence that the progress of atherosclerosis can be halted and the clinical sequelae can be reduced. The newly available results from more recent intervention studies have reinforced the validity of this conclusion. The intervention studies reduced the CHD incidence rate by approximately 2% for every 1% reduction in total cholesterol (TC) even though the studies were of relatively short duration (typically 5 years). More prolonged exposure to lower TC levels can be expected to yield even greater ultimate benefit. The benefit is most clearcut for men at highest risk. The combined data indicate that both fatal and nonfatal CHD can be reduced. More data on the extremes of age, on subjects with moderate elevations of TC, and on women would be valuable, but it is reasonable to proceed with advice to the general population aimed at reducing average cholesterol levels, and also to identify and treat those at high risk. There is good reason to expect that these measures will further reduce MI events and in all likelihood also MI deaths. Whether they will also reduce overall mortality is at present a moot point; however, a reduction in the burden of nonfatal MI would in itself be a very desirable objective. |
| Does measurement of apolipoprotein B have a place in cholesterol management? Vega, G. L. and S. M. Grundy (1990), Arteriosclerosis 10(5): 668-71. |
| Does plasma cholesterol concentration predict mortality from coronary heart disease in elderly people? 18 year follow up in Whitehall study Shipley, M. J., S. J. Pocock, et al. (1991), Bmj 303(6794): 89-92. Abstract: OBJECTIVE--To explore the extent to which the relation between plasma cholesterol concentration and risk of death from coronary heart disease in men persists into old age. DESIGN--18 year follow up of male Whitehall civil servants. Plasma cholesterol concentrations and other risk factors were determined at first examination in 1967-9 when they were aged 40-69. Death of men up to 31 January 1987 was recorded. SUBJECTS--18,296 male civil servants, 4155 of whom died during follow up. MAIN OUTCOME MEASURES--Cause and age of death. Cholesterol concentration in 1967-9 and number of years elapsed between testing and death. RESULTS--1676 men died of coronary heart disease. The mean cholesterol concentration in these men was 0.32 mmol/l higher than that in all other men (95% confidence interval 0.26 to 0.37 mmol/l). This difference in cholesterol concentrations fell 0.15 mmol/l with every 10 years' increase in age at screening. The risk of raised cholesterol concentration fell with age at death. Compared with other men cholesterol concentration in those who died of coronary heart disease was 0.44 mmol/l higher in those who died aged less than 60 and 0.26 mmol/l higher in those aged 60-79 (p = 0.03). For a given age at death the longer the gap between cholesterol measurement and death the more predictive the cholesterol concentration, both for coronary heart disease and all cause mortality (trend test p = 0.06 and 0.03 respectively). CONCLUSION--Reducing plasma cholesterol concentrations in middle age may influence the risk of death from coronary heart disease in old age. |