| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Tyrosine 192 in apolipoprotein A-I is the major site of nitration and chlorination by myeloperoxidase, but only chlorination markedly impairs ABCA1-dependent cholesterol transport Shao, B., C. Bergt, et al. (2005), J Biol Chem 280(7): 5983-93. Abstract: High density lipoprotein (HDL) isolated from human atherosclerotic lesions and the blood of patients with established coronary artery disease contains elevated levels of 3-nitrotyrosine and 3-chlorotyrosine. Myeloperoxidase (MPO) is the only known source of 3-chlorotyrosine in humans, indicating that MPO oxidizes HDL in vivo. In the current studies, we used tandem mass spectrometry to identify the major sites of tyrosine oxidation when lipid-free apolipoprotein A-I (apoA-I), the major protein of HDL, was exposed to MPO or peroxynitrite (ONOO(-)). Tyrosine 192 was the predominant site of both nitration and chlorination by MPO and was also the major site of nitration by ONOO(-). Electron paramagnetic spin resonance studies of spin-labeled apoA-I revealed that residue 192 was located in an unusually hydrophilic environment. Moreover, the environment of residue 192 became much more hydrophobic when apoA-I was incorporated into discoidal HDL, and Tyr(192) of HDL-associated apoA-I was a poor substrate for nitration by both myeloperoxidase and ONOO(-), suggesting that solvent accessibility accounted in part for the reactivity of Tyr(192). The ability of lipid-free apoA-I to facilitate ATP-binding cassette transporter A1 cholesterol transport was greatly reduced after chlorination by MPO. Loss of activity occurred in concert with chlorination of Tyr(192). Both ONOO(-) and MPO nitrated Tyr(192) in high yield, but unlike chlorination, nitration minimally affected the ability of apoA-I to promote cholesterol efflux from cells. Our results indicate that Tyr(192) is the predominant site of nitration and chlorination when MPO or ONOO(-) oxidizes lipid-free apoA-I but that only chlorination markedly reduces the cholesterol efflux activity of apoA-I. This impaired biological activity of chlorinated apoA-I suggests that MPO-mediated oxidation of HDL might contribute to the link between inflammation and cardiovascular disease. |
| U18666A inhibits intracellular cholesterol transport and neurotransmitter release in human neuroblastoma cells Sparrow, S. M., J. M. Carter, et al. (1999), Neurochem Res 24(1): 69-77. Abstract: To determine if neurochemical function might be impaired in cell models with altered cholesterol balance, we studied the effects of U18666A (3-beta-(2-diethyl-amino)ethoxyandrost-5-en-17-one) on intracellular cholesterol metabolism in three human neuroblastoma cell lines (SK-N-SH, SK-N-MC, and SH-SY5Y). U18666A (< or =0.2 microg/ml) completely inhibited low density lipoprotein (LDL)-stimulated cholesterol esterification in SK-N-SH cells, while cholesterol esterification stimulated by 25-hydroxycholesterol or bacterial sphingomyelinase was unaffected or partially inhibited, respectively. U18666A also blocked LDL-stimulated downregulation of LDL receptor and caused lysosomal accumulation of cholesterol as measured by filipin staining. U18666A treatment for 18 h resulted in 70% inhibition of K+-evoked norepinephrine release in phorbol ester-differentiated SH-SY5Y cells, while release stimulated by the calcium ionophore A23187 was only slightly affected. These results suggest that U 18666A may preferentially block a voltage-regulated Ca2+ channel involved in norepinephrine release and that alterations in neurotransmitter secretion might be a feature of disorders such as Niemann-Pick Type C, in which intracellular cholesterol transport and distribution are impaired. |
| U-73482: a novel ACAT inhibitor that elevates HDL-cholesterol, lowers plasma triglyceride and facilitates hepatic cholesterol mobilization in the rat Bell, F. P., R. B. Gammill, et al. (1992), Atherosclerosis 92(2-3): 115-22. Abstract: U-73482, a novel acylCoA:cholesterol acyltransferase (ACAT) inhibitor with systemic activity, has been evaluated for its effects on a variety of lipid metabolic parameters in the rat. The compound inhibits ACAT in vitro in cultured Fu5AH rat hepatoma cells and demonstrates systemic activity through inhibition of hepatic ACAT in rats receiving the drug orally. U-73482 also lowers plasma triglycerides at 40 mg/kg per day in the rat and elevates high density lipoprotein cholesterol (HDL-chol) in a dose-related fashion over the range of daily intakes of 0-40 mg/kg in the rat. Elevations in HDL-chol are followed by elevations in total plasma cholesterol in normal rats but the compound exerts hypocholesterolemic activity in cholesterol-fed rats and promotes clearance of stored hepatic sterol in rats pretreated with a hypercholesterolemic diet and then changed over to normal chow. The triglyceride-lowering and HDL-chol elevating effects of U-73482 coupled with its ability to promote tissue sterol clearance and block the hypercholesterolemic effects of dietary cholesterol in animals, suggests that the compound has potential as a therapeutic agent for treatment of lipid disorders in man. |
| Ubiquinone, dolichol, and cholesterol metabolism in aging and Alzheimer's disease Edlund, C., M. Soderberg, et al. (1992), Biochem Cell Biol 70(6): 422-8. Abstract: The lipid compositions of various regions of the human brain were investigated during aging and in Alzheimer's disease. The phospholipid amounts and compositions remained unchanged during aging. There were, however, considerable differences both in phospholipid composition and amount when the various regions were compared. The level of dolichol increased severalfold in all regions up to the age of 70, but there was no further elevation thereafter. The ubiquinone level decreased significantly in all parts of the brain upon aging. In Alzheimer's disease, the dolichol level was decreased in all regions, and particularly, in those affected by the disease. In contrast, the dolichyl-P concentration increased in those regions that exhibited morphological changes. There was no modification in cholesterol distribution, but a significant elevation in ubiquinone content was observed in most regions. The only phospholipid whose level was elevated was phosphatidylinositol, and only in those parts of the brain that were affected. The content of polyunsaturated fatty acids in phosphatidylethanolamine was greatly decreased in connection with the disease, with a parallel increase in the saturated portion. The results indicate that Alzheimer's disease results in specific and significant changes in the levels of lipid products of the mevalonate pathway in the brain. |
| Ultracentrifugation systematically overestimates vesicular cholesterol levels in bile Yuet, P. K., D. Blankschtein, et al. (1996), Hepatology 23(4): 896-903. Abstract: To accurately determine the cholesterol (Ch) distribution between mixed micelles and vesicles in lithogenic bile, both ultracentrifugation and gel chromatography with the correct intermixed micellar/vesicular bile salt concentration (IMC) have been proposed. We have systematically compared both separation techniques with physiological model biles to ascertain their quantitative separation ability. After determination of optimal ultra-centrifugation conditions in systems containing only micelles or vesicles, Ch-supersaturated model biles 3-10 g/dL, 10 mol percent Ch, taurocholate (TC)/(TC + egg yolk phosphatidylcholine (EYPC) = 0.6 and 0.7) were adjusted to a density of 1.03 g/mL, and ultracentrifuged at 42,000 rpm and 37 degrees C for 13 hours. Identical model biles were subjected to gel chromatography with the correct IMC, either directly or after remixing and incubation at 37 degrees C after ultracentrifugation. By ultracentrifugation, 31 percent +/- 2 percent (TC/(TC + EYPC) = 0.6) and 40 percent +/- 5 percent (TC/(TC + EYPC) = 0.7) of total Ch were found in vesicles (Ch/EYPC molar ratios = 1.0 and 1.3, respectively). However, by gel chromatography, only 19 percent +/- 2 percent (Ch/EYPC = 1.0) and 22 percent +/- 2 percent (Ch/EYPC = 1.5) of total Ch were found in the corresponding biles. Gel chromatography of biles (TC/(TC + EYPC) = 0.7) ultracentrifuged for various durations showed a progressive increase in vesicular Ch to 41 percent after 13 hours. On incubation for 11.5 hours after ultracentrifugation, vesicular Ch decreased to 31 percent, thus approaching the initial (gel chromatography) value. Quasielastic light scattering also demonstrated formation of vesicles in ultracentrifuged Ch-unsaturated model bile (cholesterol saturation index (CSI) approximately 0.97). As compared with gel chromatography, ultracentrifugation systematically elevates vesicular Ch, possibly because of induced shifts in lipids between lipid aggregates caused by variation in local bile salt concentration. Because ultracentrifugation can alter the phases present in bile, gel chromatography with the correct IMC more accurately represents the distribution of Ch in biliary lipid aggregates. |
| Ultrastructural detection of cholesterol in the liver in chronic alcoholic intoxication Loginov, A. S. and V. V. Ul'ianova (1990), Biull Eksp Biol Med 109(6): 619-21. Abstract: The authors studied the deposits of cholesterol in the liver of alcoholic men and rats by means of cytochemical method. The localization of cholesterol in intracellular and extracellular compartments was shown. In numerous hepatocytes there were focal destructions in mitochondria, rough endoplasmic reticulum and plasma membranes. |
| Ultrastructural detection of cholesterol in the liver of rats with alcoholic intoxication Ul'ianova, V. V., L. V. Molostova, et al. (1990), Biull Eksp Biol Med 109(5): 510-2. Abstract: The deposits of cholesterol in hepatocytes in alcoholic rats were studied by means of cytochemical method. It was shown the localization of cholesterol in intracellular as well as extracellular compartment. In numerous hepatocytes there was observed a destruction of mitochondria, rough endoplasmic reticulum and plasma membranes. It was observed two structural forms of digitonin cholesterol complexes: structures like "crinkles" and small cylinders and multilamellar ones. |
| Ultrastructural localization of flotillin-1 to cholesterol-rich membrane microdomains, rafts, in rat brain tissue Kokubo, H., J. B. Helms, et al. (2003), Brain Res 965(1-2): 83-90. Abstract: There is much interest in research on cholesterol-rich membrane microdomains, rafts, in the field of neurobiology. However, no one has shown the ultrastructure of rafts in tissues. We examined the ultrastructure of rafts in rat brain tissue by pre-embedding immunoelectron microscopy using flotillin-1 antibody, which is a biochemical marker of lipid rafts, and BCtheta, which is nicked and biotinylated theta-toxin, and binds to membrane cholesterol of rafts. Flotillin-1- and BCtheta-labeled areas were patchy and prominent on the plasma membranes of small processes and synapses in the neuropil. The size of flotillin-1 labeling was 40-200 nm. In addition, the membrane of lysosome and Golgi apparatus were frequently labeled for flotillin-1 with a patchy pattern. Flotillin-1 and BCtheta were mostly colocalized in double immunolabeling on a part of the plasma membranes of small processes and secondary lysosome membranes. We first indicate that flotillin-1 localizes to BCtheta-positive cholesterol-rich membrane microdomains in vivo, and that flotillin-1 and BCtheta could be ultrastructural raft markers in neural tissue. |
| Ultrastructural study of echinocytes induced by poly (ethylene glycol)-cholesterol Baba, T., N. Terada, et al. (2004), Histochem Cell Biol 122(6): 587-92. Abstract: Poly (ethylene glycol)-cholesterol (PEG-Chol) consists of a hydrophilic PEG and hydrophobic cholesterol moiety. When PEG-Chol was applied to erythrocytes, the reagent quantitatively induced protrusions by exclusively distributing in the outer monolayer of the membrane. This kind of response has been regarded as a general response that reduces the stress of expansion of the outer monolayer. However, the relationship between the membrane architecture and the distribution of such molecules is unknown. In this study, we examined the distribution of tagged PEG-Chol along the shape change pathway. The echinocytic shape was initiated by the initial formation of bumps on the rim of the discoid, which subsequently elongated as protrusions. These protrusions contained aggregates of granular structures, which appeared to accommodate the increase in the outer monolayer area. At higher concentrations, PEG-Chol further induced sphero-echinocytosis that resulted in numerous branched protrusion processes. We found that PEG-Chol was exclusively distributed in these protrusions and, in particular, accumulated at the tips. These results suggested that externally intercalated PEG-Chol was sequestrated from erythrocytes as membrane protrusions through an as-yet-unknown mechanism. |
| Ultrastructure of cholesterol gallstones as observed by electron microscopy after freeze-fracturing Abe, A., Y. Tsuchiya, et al. (1997), Tissue Cell 29(2): 191-7. Abstract: The ultrastructure of cholesterol gallstones (mixed type) was studied in detail for the first time under the transmission electron microscope after freeze-fracturing. Gallstones consisted essentially of cholesterol crystals, some impurities, and fluid. In accord with the theoretical 3.4 nm bilayered structure of cholesterol crystals, 3-4 nm periodicity of crystal layering was observed. However, gallstone cholesterol crystals were not perfect and often showed structural defects. Between crystals, complete edge-to-surface, edge-to-edge and surface-to-surface adhesions, and overall block-like aggregations were found. These may represent the structural basis for the stability of cholesterol crystal aggregation. The easy breakdown of cholesterol gallstones by extracorporeal shock wave lithotripsy is discussed in relation to their ultrastructure. |
| Unbalanced diet to lower serum cholesterol level is a risk factor for postmenopausal osteoporosis and distal forearm fracture Varenna, M., L. Binelli, et al. (2001), Osteoporos Int 12(4): 296-301. Abstract: The purpose of this study was to assess whether dietary changes aimed at reducing serum cholesterol can increase the risk of osteoporosis (OP) and fracture. The study group consisted of 311 postmenopausal women with high serum cholesterol levels and following a diet low in dairy products (calcium intake estimated at less than 300 mg/day) for 27.3 +/- 29.1 months. This sample was compared with a case-control group of 622 healthy postmenopausal women paired for age and age at menopause and with a calcium intake estimated at more than 1 g/day. Bone mineral density was measured at the lumbar spine by dual-energy X-ray absorptiometry. Prevalence of OP was significantly higher in women with a low dairy calcium intake (42.1% vs 22.3%; p < 0.0001), as was the number of Colles' fractures occurring after menopause (4.5% vs 1.6%; p = 0.008). Multiple logistic regression analyses demonstrated that a diet low in dairy calcium was a risk factor for OP (OR = 2.52, 95% CI 1.84-3.45) and Colles' fracture (OR = 2.72, 95% CI 1.18-6.26). In the low dairy calcium group, diet duration significantly influenced the risk of OP (OR = 1.13, 95% CI 1.01-1.25 for 1 year of diet). No differences in further risk factors for coronary heart disease were found between the groups, but the proportion of women physically active was lower in the women with high serum cholesterol levels. A diet that severely limits calcium intake from dairy products in an attempt to correct raised serum cholesterol levels is a risk factor for postmenopausal OP and Colles' fracture. Dietary intervention methods to lower serum cholesterol in postmenopausal women should maintain an adequate calcium intake by providing calcium from low-fat dairy products or calcium supplements. |
| Unconjugated bilirubin and cholesterol gallstone formation Ostrow, J. D. (1990), Hepatology 12(3 Pt 2): 219S-224S; discussion 224S-226S. Abstract: Cholesterol gallstones usually have small amounts of pigment at their centers and often have diffuse pigmentation or pigmented layers alternating with cholesterol layers and/or pigmented rims associated with calcium carbonate (eggshell calcification). The pigments are primarily monomeric calcium salts of unconjugated bilirubin anions and/or an insoluble, black, network polymer of tetrapyrroles. Bilirubin presumably can precipitate only if bile is supersaturated with calcium bilirubinates. Among various in vitro model systems, the aqueous solubilities and pK'a values for unconjugated bilirubin differ greatly. It is therefore not known whether normal bile is saturated with unconjugated bilirubin. However, all systems indicate that unconjugated bilirubin is solubilized by binding to bile salt monomers and oligomers, as well as micelles; marked metastable supersaturation of unconjugated bilirubin can occur in the presence of bile salt micelles, and both pK'a values of unconjugated bilirubin are greater than 6.0, probably because of internal hydrogen-bonding of the--COOH groups. Lecithin decreases equilibrium solubilization of unconjugated bilirubin crystals but enhances metastable supersaturation of unconjugated bilirubin. Calcium ions form insoluble salts with unconjugated bilirubin monoanions and dianions but soluble complexes with bilirubin conjugates. The solubility products of the calcium bilirubinate salts suggest that normal hepatic bile is not saturated with CaB or Ca(HB)2 but that gallbladder bile may be supersaturated with Ca(HB)2.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Unconjugated bilirubin in human bile: the nucleating factor in cholesterol cholelithiasis? Dutt, M. K., G. M. Murphy, et al. (2003), J Clin Pathol 56(8): 596-8. Abstract: AIMS: To investigate the concentrations of bilirubin, bilirubin conjugates, phospholipid, and cholesterol in the gall bladder bile obtained at surgery from patients with and without cholesterol gallstones. METHODS: Gall bladder bile was collected during surgery, by puncture, from 20 patients with gallstones undergoing routine cholecystectomy and from eight patients with normal liver blood tests. Concentrations of bilirubin, bilirubin conjugates, phospholipid, and cholesterol were measured using standard procedures. RESULTS: The proportion of total bilirubin that was unconjugated was significantly higher in the bile from patients with stones than in bile from control patients, whether or not the bile from either group was saturated with cholesterol or not. Indeed, the mean concentration of cholesterol was significantly higher in control bile samples. CONCLUSION: The presence of stones was more closely related to the proportion of unconjugated bilirubin than to the degree of saturation of bile with cholesterol. Bilirubin and its metabolites probably play an important part in the formation of cholesterol gallstones. |
| Uncoupling of biliary phospholipid and cholesterol secretion in mice with reduced expression of mdr2 P-glycoprotein Oude Elferink, R. P., R. Ottenhoff, et al. (1996), J Lipid Res 37(5): 1065-75. Abstract: Mice in which the gene for mdr2 P-glycoprotein has been disrupted have a severe deficiency in biliary phospholipid and cholesterol secretion. We studied the relation between mdr2 gene expression and biliary lipid secretion with emphasis on the role of bile salt hydrophobicity. Control mice (+/+), and mice with a homozygous (-/-) or heterozygous (+/-) disruption of the mdr2 gene, were infused with taurodeoxycholate (TDC) or tauroursodeoxycholate (TUDC). In mdr2 (-/-) mice, virtually no phospholipids were secreted into bile, irrespective of the type of bile salt infused. In contrast, cholesterol secretion in (-/-) mice increased upon TDC infusion from less than 0.1 to more than 2 nmol/min. 100 g, which was similar to controls under the same conditions. After infusion of TUDC in (-/-) mice. cholesterol secretion also rose (to 1.8 nmol/min. 100 g) but remained much lower than in controls (8 nmol/min x 100 g). In (+/-) mice, cholesterol secretion was equal to (+/+) mice during secretion of endogenous bile salts and during TDC infusion, but was 50% of control levels during maximal TUDC infusion. We conclude that biliary phospholipid secretion completely depends on mdr2 gene expression but cholesterol can, at least partially, be secreted in an mdr2 Pgp-independent mechanism. The extent to which cholesterol is secreted via this mechanism may depend on the hydrophobicity (i.e., cholesterol-solubilizing capacity) of the secreted bile salt. |
| Uncoupling of the cholera toxin-G(M1) ganglioside receptor complex from endocytosis, retrograde Golgi trafficking, and downstream signal transduction by depletion of membrane cholesterol Wolf, A. A., Y. Fujinaga, et al. (2002), J Biol Chem 277(18): 16249-56. Abstract: To induce toxicity, cholera toxin (CT) must first bind ganglioside G(M1) at the plasma membrane, enter the cell by endocytosis, and then traffic retrograde into the endoplasmic reticulum. We recently proposed that G(M1) provides the sorting motif necessary for retrograde trafficking into the biosynthetic/secretory pathway of host cells, and that such trafficking depends on association with lipid rafts and lipid raft function. To test this idea, we examined whether CT action in human intestinal T84 cells depends on membrane cholesterol. Chelation of cholesterol with 2-hydroxypropyl beta-cyclodextrin or methyl beta-cyclodextrin reversibly inhibited CT-induced chloride secretion and prolonged the time required for CT to enter the cell and induce toxicity. These effects were specific to CT, as identical conditions did not alter the potency or toxicity of anthrax edema toxin that enters the cell by another mechanism. We found that endocytosis and trafficking of CT into the Golgi apparatus depended on membrane cholesterol. Cholesterol depletion also changed the density and specific protein content of CT-associated lipid raft fractions but did not entirely displace the CT-G(M1) complex from these lipid raft microdomains. Taken together these data imply that cholesterol may function to couple the CT-G(M1) complex with raft domains and with other membrane components of the lipid raft required for CT entry into the cell. |
| Uncritical review of articles on cholesterol Ravnskov, U. (1994), Ugeskr Laeger 156(31): 4479-80. |
| Underestimation of the importance of blood pressure and cholesterol for coronary heart disease mortality in old age Clarke, R., S. Lewington, et al. (2002), Eur Heart J 23(4): 286-93. Abstract: AIMS: To take appropriate account of duration of follow-up in estimating age-specific associations of 'usual' blood pressure and cholesterol with death from coronary heart disease. METHODS and RESULTS: Blood pressure and cholesterol were measured in 18 841 men at entry to the Whitehall study, and coronary heart disease mortality was recorded during a 26-year period. Biennial re-measurements of these risk factors in the Framingham study were used to obtain period-specific corrections for 'regression dilution'. For coronary heart disease deaths at ages 40-64, 65-74 and 75+ years in the Whitehall study, the mean times since baseline were 9, 15, and 21 years, respectively. In uncorrected analyses of coronary heart disease risk in each age range, a 10 mmHg lower systolic blood pressure at baseline was associated with proportional risk reductions of only 19%, 14% and 10%, respectively (P<0.001 for trend with age). After period-specific correction for regression dilution, a 10 mmHg lower usual systolic blood pressure about 5 years before coronary heart disease death was associated with risk reductions of 25%, 23% and 21%, respectively (trend P=0.1). Similarly, a 1 mmol. l(-1)lower blood cholesterol was associated with proportional reductions in coronary heart disease risk of 21%, 17% and 11% (trend P<0.001) in uncorrected analyses, by contrast with proportional reductions of 27%, 26% and 21% (trend P=0.5) after period-specific correction. CONCLUSIONS: After making appropriate allowance for the longer interval between baseline measurements and death at older ages, reductions in the risk of coronary heart disease death associated with differences in usual levels of blood pressure or cholesterol at some particular fixed time prior to death were about as great in old age as in middle age. |
| Underlying mechanisms in the development and progression of cholesterol cholelithiasis Mansurov, K. (1991), Klin Med (Mosk) 69(9): 17-21. |
| Understanding lipoproteins as transporters of cholesterol and other lipids Biggerstaff, K. D. and J. S. Wooten (2004), Adv Physiol Educ 28(1-4): 105-6. Abstract: A clear picture of lipoprotein metabolism is essential for understanding the pathophysiology of atherosclerosis. Many students are taught that low-density lipoprotein-cholesterol is "bad" and high-density lipoprotein-cholesterol is "good." This misconception leads to students thinking that lipoproteins are types of cholesterol rather than transporters of lipid. Describing lipoproteins as particles that are composed of lipid and protein and illustrating the variation in particle density that is determined by the constantly changing lipid and protein composition clarifies the metabolic pathway and physiological function of lipoproteins as lipid transporters. Such a description will also suggest the critical role played by apolipoproteins in lipid transport. The clarification of lipoproteins as particles that change density will help students understand the nomenclature used to classify lipoproteins as well. |
| Understanding physician and consumer attitudes concerning cholesterol management: results from the National Lipid Association surveys Pasternak, R. C., J. M. McKenney, et al. (2004), Am J Cardiol 94(9A): 9F-15F. Abstract: Two online surveys commissioned by the National Lipid Association (NLA) were conducted to determine the current attitudes of physicians and consumers regarding cholesterol and heart disease. Physicians and consumers from preexisting independent panels were randomly invited to participate in the online surveys that were open from January 26 to 30, 2004. Both physicians (n = 200) and consumers (n = 600) agreed that high cholesterol and coronary artery disease (CAD) are significant health risks. Physicians reported the primary barriers for patients being prescribed cholesterol-lowering medication as patient fear of side effects (61%) and reluctance to take prescription medications (52%). While most physicians were aware of and felt they adhered to the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) guidelines, considerably fewer thought the same of other physicians. The consumer survey focused on untreated moderate-risk patients (an approximate 10% to 20% 10-year risk of myocardial infarction and cardiac death) because this group is often undertreated. Untreated moderate-risk patients reported that their physicians did not advise them to take prescription cholesterol-lowering drugs (51%) and that they were trying to control their cholesterol with diet and exercise (58%). Consumers believe they are taking an increased role in their own health management and decision making. Current attitudes of physicians and consumers are similar with regard to their recognition of the significance of cholesterol and CAD for health, but differ with regard to why patients do not take prescription medications. |