| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Cholesterol and coronary heart disease: predicting risks in men by changes in levels and ratios Kinosian, B., H. Glick, et al. (1995), J Investig Med 43(5): 443-50. Abstract: BACKGROUND: Little is known about the relative ability of different measures of change in cholesterol to discriminate coronary heart disease risk. We evaluated this ability for changes in low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, LDL/HDL ratios, and total cholesterol/HDL ratios. METHODS: We predicted risks of coronary heart disease using data from 3641 men in the Lipid Research Clinics Coronary Primary Prevention Trial. Treating these patients as a cohort, we estimated risks associated with changes in cholesterol levels independent of the patients' randomization group. RESULTS: Changes in LDL and HDL cholesterol when used in combination were each significant predictors of coronary heart disease risk (odds ratios OR for 10% increases, 1.15 and 0.84, respectively; P < 0.001). Changes in LDL/HDL and total cholesterol/HDL ratios had similar discriminating ability (OR for 10% increases, 1.17 and 1.21, respectively; P < 0.0001). In the best discriminating models, changes in ratios added information about risks to changes in LDL cholesterol, although changes in LDL cholesterol levels failed to add information to changes in ratios. CONCLUSIONS: Changes in total cholesterol/HDL and LDL/HDL ratios were better predictors of risk for coronary heart disease than were changes in LDL cholesterol levels alone. When assessed as percentage changes averaged during the first two months of intervention, they were among the best discriminators of risk. Clinicians selecting treatments for intervention should include among their considerations the treatment's effect on both LDL and HDL cholesterol rather than their effects on LDL cholesterol levels alone. |
| Cholesterol and coronary heart disease: screening and treatment Turner-Boutle, M. (1998), Nurs Times 94(15): 46-7. Abstract: The prevention of coronary heart disease would represent a major saving to the NHS. Systematic review of evidence relating to screening for CHD and its prevention suggests that blood cholesterol measurement on its own is a poor predictor of risk. The evidence suggests that lifestyle changes and drug treatments other than cholesterol-lowering drugs are the most cost-effective approach to prevention. Nurses should ensure that all risk factors are assessed and a range of preventive measures considered in situations where CHD is a potential risk. |
| Cholesterol and coronary ischemia Jorquera Plaza, F. and J. M. Culebras Fernandez (1995), Nutr Hosp 10(3): 141-2. |
| Cholesterol and coronary sclerosis Immich, H. (1997), Versicherungsmedizin 49(3): 86-8. Abstract: This paper defines the terms logic, cause, and risk. Furthermore this paper shows; High serum cholesterol concentrations do not cause the sclerosis of the coronary arteries. Therefore, interventions are useless. |
| Cholesterol and depression Ernst, E., T. Saradeth, et al. (1994), Arch Intern Med 154(10): 1166. |
| Cholesterol and development Roux, C., C. Wolf, et al. (1997), C R Seances Soc Biol Fil 191(1): 113-23. Abstract: The teratogenic action of distal inhibitors of cholesterol synthesis has been known for some time. The induced malformations are of a particular type: they include holoprosencephalies. Recently these observations have solicited increased interest due to: 1/ the discovery in 1993 of a similar form of inhibition of cholesterol synthesis which is responsible for a human malformation syndrome, Smith-Lemli-Opitz; 2/ the demonstration of the involvement of the Sonic Hedgehog gene in normal development of prosencephalon and the description of the mode of action of the protein Shh: autoprocessing followed by "cholesterolisation". |
| Cholesterol and development: the RSH ("Smith-Lemli-Opitz") syndrome and related conditions Opitz, J. M., E. Gilbert-Barness, et al. (2002), Pediatr Pathol Mol Med 21(2): 153-81. Abstract: The half-century of lipophobia in the United States may be abating with some return of sanity on the discussion of health and dietary fat Taubes, 2001. The youngest victims of this collective, decades long madness are those infants deprived for one reason or another of breast milk. They are unable to speak for themselves at a time of greatest need for cholesterol during growth, the most critical period of myelination of central and peripheral nervous system, formation of bone and bile, and of every steroid hormone. Some of the commercial formulas they are fed contain only 1 or 2 mg of cholesterol per 100 g edible portion contrasted with almost 14 mg in breast milk. One can only hope that the confidence in their endogenous ability to synthesize sufficient amounts of cholesterol is not misplaced. Pediatric pathology has learned that when this endogenous ability fails during embryogenesis on the basis of mutations in the postsqualene biosynthesis of cholesterol, a startling variety of developmental pathology may present itself ranging from lethal forms of "idiopathic" hydrops, microcephaly with cerebral dysgenesis and dysmyelinization, agenesis of corpus callosum, cerebellar vermis dysgenesis, cataracts, cleft palate, many different forms of congenital heart defect, pyloric stenosis and/or Hirschsprung dysganglionosis, adrenal (cortical) insufficiency, cholestatic liver disease, limb malformations, and genital ambiguity in genetic males. Population genetic considerations suggest a hypothetical birth prevalence of the RSH (so-called Smith-Lemli-Opitz) syndrome, the commonest of these Garrodian errors of cholesterol biosynthesis, of 1/2500; since only about 1/15,000 to 1/20,000 homozygotes are liveborn and biochemically confirmed, over 80% prenatal or perinatal mortality must occur and deserves the most discerning of services from birth attendants, perinatologists, neonatologists, and fetal/pediatric pathologists. An easy, reliable, economical biochemical test for the presence of 7-dehydrocholesterol is available and the commonest mutation, the IVS8-1G-->C mutation, is quickly and reliably tested for molecularly. Thus, the successful diagnosis, even after death, will contribute substantially to correct genetic counseling, carrier detection, prenatal diagnosis, and treatment in those known to be affected prenatally andplanned to be liveborn. Thus, developmental pathology plays an integral, vital role in preventive medicine. |
| Cholesterol and diseases of the cardiovascular system. Skeptical opinions Ceremuzynski, L. and B. Bednarz (1991), Kardiol Pol 35(8): 91-4. |
| Cholesterol and ergosterol influence nystatin surface aggregation: relation to pore formation Coutinho, A., L. Silva, et al. (2004), Biophys J 87(5): 3264-76. Abstract: Nystatin interaction with liposomes mimicking fungal and mammalian membranes (ergosterol- and cholesterol-containing 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC) large unilamellar vesicles, respectively) was studied by fluorescence spectroscopy. The activity of this antibiotic was also measured using a pyranine fluorescence detected K+/H+ exchange assay. Nystatin mean fluorescence lifetime varied with the antibiotic concentration and ergosterol content (0-30 mol%) of the lipid vesicles. It sharply increased from 5 to 37 ns upon reaching 100 molecules per liposome, reporting nystatin oligomerization in the membrane. Concomitantly, spectral alterations typical of excitonic coupling were detected and there was a pronounced increase in the initial rate of pore formation by nystatin. These findings suggest that nystatin exerts its antibiotic activity via a two-stage mechanism: at low antibiotic concentrations, surface-adsorbed monomeric antibiotic molecules perturb the lipid packing, changing the permeability properties of the ergosterol-rich liposomes. Upon reaching a critical threshold, nystatin mode of action switches to the classical model of transmembrane aqueous channel formation. In the presence of cholesterol-containing POPC liposomes, neither nystatin spectroscopic properties, nor the kinetics of K+ efflux varied with the antibiotic concentration suggesting that in this case the first stage of antibiotic mode of action always prevails or the assemblies formed by nystatin and cholesterol are very loose. |
| Cholesterol and ergosterol superlattices in three-component liquid crystalline lipid bilayers as revealed by dehydroergosterol fluorescence Liu, F., I. P. Sugar, et al. (1997), Biophys J 72(5): 2243-54. Abstract: We have examined the fractional sterol concentration dependence of dehydroergosterol (DHE) fluorescence in DHE/cholesterol/dimyristoyl-L-alpha-phosphatidylcholine (DMPC), DHE/ergosterol/DMPC and DHE/cholesterol/dipalmitoyl-L-alpha-phosphatidylcholine (DPPC) liquid-crystalline bilayers. Fluorescence intensity and lifetime exhibit local minima (dips) whenever the total sterol mole fraction, irrespective of the DHE content, is near the critical mole fractions predicted for sterols being regularly distributed in hexagonal superlattices. This result provides evidence that all three of these naturally occurring sterols (e.g., cholesterol, ergosterol, and DHE) can be regularly distributed in the membrane and that the bulky tetracyclic ring of the sterols is the cause of regular distribution. Moreover, at the critical sterol mole fractions, the steady-state anisotropy of DHE fluorescence and the calculated rotational relaxation times exhibit distinct peaks, suggesting that membrane free volume reaches a local minimum at critical sterol mole fractions. This, combined with the well-known sterol condensing effect on lipid acyl chains, provides a new understanding of how variations in membrane sterol content change membrane free volume. In addition to the fluorescence dips/peaks corresponding to hexagonal superlattices, we have observed intermediate fluorescence dips/peaks at concentrations predicted by the centered rectangular superlattice model. However, the 22.2 mol% dip for centered rectangular superlattices in DHE/ergosterol/DMPC mixtures becomes diminished after long incubation (4 weeks), whereas on the same time frame the 22.2 mol% dip in DHE/cholesterol/DMPC mixtures remains discernible, suggesting that although all three of these sterols can be regularly distributed, subtle differences in sterol structure cause changes in lateral sterol organization in the membrane. |
| Cholesterol and fatty acid metabolism in piglets fed sow milk or infant formula with or without addition of cholesterol Rioux, F. M. and S. M. Innis (1993), Metabolism 42(12): 1552-9. Abstract: Several studies have reported that plasma cholesterol and phospholipid (PL) levels of arachidonic acid (20:4n-6) are lower and PL levels of linoleic acid (18:2n-6) are higher in infants fed formula than in infants fed human milk. Plasma cholesterol level and possibly the dietary intake of cholesterol could be related to plasma PLn-6 fatty acid metabolism because plasma PL 18:2n-6 is used for esterification of plasma free cholesterol. Whether the low cholesterol content of infant formula as compared with human milk is related to the difference in plasma n-6 fatty acid levels between infants fed human milk and infants fed formula is not known. This study determined the effect of feeding formula with 0.05 mmol cholesterol/L, formula with 1.09 mmol cholesterol/L, or sow milk with 0.34 mmol cholesterol/L on plasma, liver, and bile lipid fatty acid levels and liver low-density lipoprotein (LDL) receptor mass in piglets. Liver microsomal 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase activity and plasma lathosterol were assayed as indices of liver and body cholesterol synthesis, respectively. Formula with or without cholesterol added, or sow milk, was fed from birth to 18 days of age. Providing cholesterol in the formula did not correct the significantly lower plasma cholesterol or plasma and liver PL 20:4n-6 levels associated with formula feeding. The liver total cholesterol and cholesteryl esters (CE), biliary bile acid, and PL concentrations were significantly higher and the liver HMG CoA reductase activity and plasma lathosterol:cholesterol ratio were significantly lower in piglets fed the formula with cholesterol than in piglets fed the formula without cholesterol added.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Cholesterol and fatty acids of the nuclei and chromatin of the rat thymus at long intervals following gamma irradiation Kulagina, T. P. (1990), Radiobiologiia 30(3): 317-20. Abstract: The content of a total fraction of free fatty acids (FFA) and cholesterol in the chromatin, nuclei and homogenate of rat thymus were studied during three months following fractionated gamma-irradiation (2 Gy X 3 at a week interval). The FFA content in the homogenate, nuclei and chromatin of rat thymus drastically increased 60 min after the last exposure. In a month, the FFA content of nuclei and chromatin dropped to control levels, whereas that of the homogenate remained high throughout the entire period of observation and sharply increased by the third month. No changes were revealed in the cholesterol content. |
| Cholesterol and fatty acids profile of Brazilian commercial chicken giblets Pereira, N. R., E. C. Muniz, et al. (2002), Arch Latinoam Nutr 52(2): 203-6. Abstract: This study was carried out to determine the chemical composition, cholesterol contents and fatty acids profile of Brazilian commercial chicken giblets. The analysis were performed in gizzard, liver and heart in natura and also in cooked gizzard, fried liver and roasted heart. Fat and cholesterol contents ranged from 0.88% and 72.68 mg/100 g, in cooked gizzard, to 22.19% and 213.18 mg/100 g, in roasted heart. As the fat content gets higher, so does the cholesterol content. Palmitic (C16:0) and stearic acids (C18:0) were the predominant saturated fatty acids (SFA). The C16:0 ranged from 6.39% in cooked gizzard to 18.51% in fried liver. The C18:0 level ranged from 6.62% in roasted heart to 19.19% in cooked gizzard. Linoleic acid (C18:2 omega 6) was the predominant polyunsaturated fatty acid (PUFA). The data revealed that the three different analysed giblets presented a good PUFA/SFA ratio, with values of 1.11, 1.14 and 1.40 for cooked gizzard, fried liver and roasted heart, respectively. |
| Cholesterol and fatty acids regulate dynamic caveolin trafficking through the Golgi complex and between the cell surface and lipid bodies Pol, A., S. Martin, et al. (2005), Mol Biol Cell 16(4): 2091-105. Abstract: Caveolins are a crucial component of plasma membrane (PM) caveolae but have also been localized to intracellular compartments, including the Golgi complex and lipid bodies. Mutant caveolins associated with human disease show aberrant trafficking to the PM and Golgi accumulation. We now show that the Golgi pool of mainly newly synthesized protein is detergent-soluble and predominantly in a monomeric state, in contrast to the surface pool. Caveolin at the PM is not recognized by specific caveolin antibodies unless PM cholesterol is depleted. Exit from the Golgi complex of wild-type caveolin-1 or -3, but not vesicular stomatitis virus-G protein, is modulated by changing cellular cholesterol levels. In contrast, a muscular dystrophy-associated mutant of caveolin-3, Cav3P104L, showed increased accumulation in the Golgi complex upon cholesterol treatment. In addition, we demonstrate that in response to fatty acid treatment caveolin can follow a previously undescribed pathway from the PM to lipid bodies and can move from lipid bodies to the PM in response to removal of fatty acids. The results suggest that cholesterol is a rate-limiting component for caveolin trafficking. Changes in caveolin flux through the exocytic pathway can therefore be an indicator of cellular cholesterol and fatty acid levels. |
| Cholesterol and fibrinogen as predictive factors of progressive carotid atherosclerosis Sanguigni, V., M. Gallu, et al. (1993), Int Angiol 12(4): 335-6. Abstract: In order to detect the presence of determining factors as predictors of progressive carotid atherosclerosis, the incidence of total serum cholesterol and fibrinogen elevation was evaluated in patients affected by coronary artery disease (CAD). 61 subjects with CAD (mean age 62 years) and significative lesions (> 50%) underwent periodic Echo-Doppler (Duplex scanning) of the supra aortic branches. Total serum cholesterol, HDL, LDL and fibrinogen were monitored, as well. A 24 month follow-up period was performed. Indicative of the progression of carotid atherosclerosis has been considered the presence of a stenosis degree over 20% than the initial one. In 14 of the 61 subjects who entered the study, there was evidence of progressive carotid atherosclerosis. The same patients showed higher levels of LDL cholesterol (130 +/- 36.3 vs 96.5 +/- 33.2) and Fibrinogen (398.3 +/- 59.4 vs 328 +/- 36.8) and lower levels of HDL cholesterol (27.2 +/- 4.2 vs 34.4 +/- 10.1). Our results confirm the importance of cholesterol and fibrinogen as determining risk factors, especially in patients with multiple vascular disease (coronary and carotid). |
| Cholesterol and glycemic effects of Niaspan in patients with type 2 diabetes Kane, M. P., R. A. Hamilton, et al. (2001), Pharmacotherapy 21(12): 1473-8. Abstract: STUDY OBJECTIVE: To determine the effect of Niaspan--a niacin preparation with both immediate- and extended-release characteristics--on lipid and glycemic control in patients with type 2 diabetes. DESIGN: Retrospective study SETTING: Private-practice endocrinology group. PATIENTS: Thirty-two patients (mean age 60 yrs; 72% men) with type 2 diabetes identified by a computerized text search. INTERVENTION: Patients received Niaspan 1000, 1500, or 2000 mg/day (median daily dosage 1000 mg). MEASUREMENTS AND MAIN RESULTS: Total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, triglycerides, hemoglobin A1c, and transaminase levels were compared for each patient before and 6 months after initiation of Niaspan. Niaspan therapy was associated with a significant 34% increase in HDL (p=0.033), a significant 36% reduction of triglycerides (p=0.049), and no significant change in LDL (p=0.236) or total cholesterol (p=0.122). Mean hemoglobin A1c levels significantly decreased from baseline by 0.5 +/- 0.3% (p=0.032), even though dosages and treatment with antidiabetic agents remained constant. There were no significant changes in transaminase levels. Seven patients (21.9%) discontinued Niaspan; one of them experienced an increase in blood glucose while receiving the agent. CONCLUSION: For most patients with type 2 diabetes, Niaspan is a safe and effective therapy for dyslipidemia and does not exacerbate glycemic control. |
| Cholesterol and health in old age: risk factor or risk marker? Harris, T. B. (2004), J Am Geriatr Soc 52(4): 639-40. |
| Cholesterol and heart disease in older persons and women. Review of an NHLBI workshop Manolio, T. A., T. A. Pearson, et al. (1992), Ann Epidemiol 2(1-2): 161-76. Abstract: The value of serum total cholesterol measurement in predicting coronary heart disease (CHD) is well established in middle-aged men, but has been questioned in middle-aged women and older people of both sexes. To address this, the most recent follow-up data from 25 populations in 22 US and international cohort studies were presented and analyzed at a recent National Heart, Lung, and Blood Institute (NHLBI) workshop. Crude relative and absolute excess risks of fatal CHD were determined for individual studies and pooled across studies to determine pooled risk estimates. Serum total cholesterol and low-density-lipoprotein (LDL) cholesterol levels predicted fatal CHD in middle-aged (< 65 years) and older (> or = 65 years) men and women, though the strength and consistency of these relationships in older women were diminished. High-density-lipoprotein (HDL) cholesterol levels inversely predicted CHD in middle-aged men and women and in older women, but not in older men. Data for minority groups and for overseas populations were similar to those for white people in the United States. Relative risk estimates were generally lower for older than for middle-aged subjects, but absolute excess risk was greater. Older people and middle-aged women with elevated cholesterol levels are clearly at increased risk of coronary disease; whether this risk can be modified by dietary or drug therapy, and at what level intervention is appropriate, must not be determined. |
| Cholesterol and hepatic lipoprotein assembly and secretion Kang, S. and R. A. Davis (2000), Biochim Biophys Acta 1529(1-3): 223-30. Abstract: The assembly and secretion of apo B100 containing lipoproteins (i.e., VLDL) by the liver and cholesterol metabolism are interrelated on several different levels and for several different physiologic reasons. Firstly, hepatic VLDL is the major precursor for LDL, which in the human is the major vehicle responsible for transporting cholesterol to peripheral tissues. Secondly, cholesterol is supplied to many tissues by a specific uptake of LDL via LDL receptor, which is expressed in a regulated manner by most mammalian tissues. Thirdly, the rate of hepatic cholesterol biosynthesis and metabolism to bile acids correlates with production of VLDL. This apparent coordinate expression of cholesterol biosynthetic/catabolic enzymes and hepatic VLDL assembly/secretion are mediated at least in part through the sterol response element binding protein (SREBP) transcription factor family. Their gene targets include a plethora of enzymes that regulate glycolysis, energy production, lipogenesis and cholesterol catabolism. Studies of hepatoma cells overexpressing CYP7A1, the rate-limiting enzyme controlling bile acid synthesis, show that as a result of increased mature SREBP1, there is a coordinate induction of lipogenesis and the assembly and secretion of VLDL. These and additional studies show that the bile acid synthetic pathway and the VLDL assembly/secretion pathway are coordinately linked through SREBP-dependent transcription. Based on studies showing that within the liver acinus, the expression of CYP7A1 is mainly in the pericentral region while HMG-CoA reductase is mainly periportal, we propose that a 'metabolic zonal segregation' plays an important role in coordinate regulation of cholesterol and VLDL metabolism. This putative 'metabolic zonal segregation' may provide segregation of metabolic functions which may be mutually antagonistic. For example, there may be physiologic states in which the bile acid synthetic pathway may compete with the VLDL assembly/secretion pathway for a limited amount of cholesterol. Metabolic antagonism (e.g., competition for cholesterol) may be avoided via inducing SREBP-mediated transcription. Adaptation of catabolic hepatocytes to accommodate the expression of VLDL assembly/secretion may occur in response to activation of SREBP-mediated transcription. Support for these is discussed. |
| Cholesterol and interleukin-6 concentrations relate to outcomes in burn-injured patients Vanni, H. E., B. R. Gordon, et al. (2003), J Burn Care Rehabil 24(3): 133-41. Abstract: The goal of this study was to determine the relationship among lipid concentrations, cytokine concentrations, and clinical outcomes of burn patients. Twenty-eight patients admitted within 24 hours of burn injury, segregated based on burn size, had blood samples drawn 24 and 48 hours after burn injury and then weekly for 3 weeks. Measurements included total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglyceride, interleukin (IL)-6, soluble IL-2 receptor, and soluble necrosis factor p55 and p75 receptors. Infection, length of stay (LOS), and survival were monitored. Cholesterol and lipoprotein concentrations decreased by at least 40% in patients with burns >20% total body surface area and inversely correlated with IL-6. Lower cholesterol and higher IL-6 values correlated with higher infection rates and longer LOS. IL-6 was the strongest predictor for LOS. In conclusion, outcomes after burn injury are related to low cholesterol and elevated IL-6 levels. |