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100 Cholesterol Studies
From 1994 to 1998
Life Flow One
The Solution For Heart Disease

by
Karl Loren

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HealthGate Document

Record 1 from database: MEDLINE
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Title

Nutritional requirements of infants and children with respect to cholesterol and related compounds.

Author

Barness LA

Address

University of South Florida College of Medicine, Tampa 33612.

Source

Am J Med Genet, 1994 May, 50:4, 353-4

Abstract

Cholesterol is an enigmatic, essential metabolite. Breast milk contains significant quantities of cholesterol, yet human infants thrive on cholesterol-free diets. Recommendations to lower serum cholesterol are widespread, yet low serum cholesterol is associated with poorly understood morbidity. Serum cholesterol is increased with diets high in fat, yet dietary cholesterol has relatively little effect on serum concentrations. Smith-Lemli-Opitz syndrome, marked with extremely low serum cholesterol, may serve as a human model for the evaluation of absorption and metabolism of dietary cholesterol.

Language of Publication

English

Unique Identifier

94270406

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MeSH Heading (Major)

Child Nutrition|*; Cholesterol|BL/*ME; Cholesterol, Dietary|*ME

MeSH Heading

Cell Membrane|CH; Child, Preschool; Human; Hypobetalipoproteinemia|PA; Infant; Infant Nutrition; Milk, Human|CH; Myelin Sheath|PH; Nutritional Requirements

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0148-7299

Country of Publication

UNITED STATES

Record 2 from database: MEDLINE
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Title

Comparable efficacy of hydrogenated versus nonhydrogenated plant sterol esters on circulating cholesterol levels in humans.

Author

Jones PJ; Ntanios F

Address

School of Dietetics and Human Nutrition, McGill University, Quebec, Canada.

Source

Nutr Rev, 1998 Aug, 56:8, 245-8

Abstract

A recent study in The Netherlands compared the effects of margarine enriched with different vegetable oil sterols with margarine containing sitostanol-ester on plasma total, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) cholesterol concentrations. Margarine with sterolesters from soybean oil (mainly esters from sitosterol, campesterol, and stigmasterol) was as effective as a margarine with sitostanol-ester in lowering blood total and LDL cholesterol levels without affecting HDL cholesterol levels.

Language of Publication

English

Unique Identifier

98406639

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MeSH Heading (Major)

Lipoproteins, HDL Cholesterol|BL/*DE; Lipoproteins, LDL Cholesterol|BL/*DE; Plant Oils|AD/*PD; Sterols|AD/*PD

MeSH Heading

Adult; Aged; Comparative Study; Double-Blind Method; Female; Human; Hydrogenation; Male; Margarine; Middle Age; Randomized Controlled Trials

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0029-6643

Country of Publication

UNITED STATES

CAS Registry/EC Number

0 (Lipoproteins, HDL Cholesterol); 0 (Lipoproteins, LDL Cholesterol); 0 (Plant Oils); 0 (Sterols); 8029-82-1 (Margarine)

Record 3 from database: MEDLINE
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Title

Epidemiologic aspects of lipid abnormalities.

Author

Criqui MH; Golomb BA

Address

University of California, San Diego, Department of Family and Preventive Medicine, La Jolla 92093-0607, USA.

Source

Am J Med, 1998 Jul 6, 105:1A, 48S-57S

Abstract

Existing cholesterol guidelines aimed at preventing cardiovascular disease emphasize the role of total cholesterol (TC) and low-density lipoprotein (LDL) cholesterol in lipid management decisions, with a subsidiary role for high-density lipoprotein (HDL) cholesterol in guiding treatment and little role for triglycerides. In this article, epidemiologic evidence is reviewed relating to the independent value of lipid factors in prediction of cardiovascular disease risk, including TC, LDL cholesterol, HDL cholesterol, very-low-density lipoprotein (VLDL) cholesterol and triglycerides, LDL particle size ("pattern B"), and the TC/HDL-cholesterol ratio. Several observations are highlighted. Triglycerides appear to be an independent risk factor in specific populations. Postprandial triglycerides may be superior to fasting triglycerides as a predictor of risk. LDL particle size does not have independent predictive value after adjustment for triglycerides. Particular emphasis is placed on the observation that the single most predictive lipid factor is the TC/HDL-cholesterol ratio, which implicitly incorporates information on both LDL and triglycerides in the numerator. This is the best predictor both of outcome and of treatment benefit, and its predictive value appears to be maintained into older age. It is concluded that increasing emphasis should be placed on the TC/HDL cholesterol ratio in epidemiologic analyses and in monitoring patients on therapy for dyslipidemia.

Language of Publication

English

Unique Identifier

98370765

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MeSH Heading (Major)

Cholesterol|*BL; Coronary Disease|BL/*ET/*MO; Hyperlipidemia|BL/*CO/*EP

MeSH Heading

Age Distribution; Age Factors; Human; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Lipoproteins, VLDL Cholesterol|BL; Risk; Sex Distribution; Sex Factors; United States|EP

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9343

Country of Publication

UNITED STATES

CAS Registry/EC Number

0 (Lipoproteins, HDL Cholesterol); 0 (Lipoproteins, LDL Cholesterol); 0 (Lipoproteins, VLDL Cholesterol); 57-88-5 (Cholesterol)

Record 4 from database: MEDLINE
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Title

Perspectives in the treatment of dyslipidemias in the prevention of coronary heart disease.

Author

Borgia MC; Medici F

Address

UniversitÄa Degli Studi di Roma La Sapienza, Italy.

Source

Angiology, 1998 May, 49:5, 339-48

Abstract

In this review the indications for the available treatments for dyslipidemias in the prevention of coronary heart disease (CHD) are considered, and their efficacy according to the latest studies is analyzed. As data sources the authors used the main multicenter studies performed in the last twenty years to evaluate primary and secondary prevention of CHD by correcting dyslipidemias as well as the results of meta-analyses of these studies. All treatments considered were found effective in preventing CHD morbidity and mortality to some extent. In particular, the combination of diet with niacin or hydroxymethylglutaryl coenzyme A (HMG CoA) reductase inhibitors seems to give the best results. These drugs induce a marked reduction of total and low-density lipoprotein (LDL) cholesterol and an increase of high-density lipoprotein (HDL) cholesterol concentrations. The use of diet, niacin, and HMG CoA reductase inhibitors reduces total as well as specific mortality. Treatment of dyslipidemia to prevent CHD depends on the pattern and severity of dyslipidemia, the presence of overt CHD, and the patient's response to diet. Pharmacologic treatment should be started only after dietary modifications have been tried and must be combined with diet. Drug side effects must also be considered, for they may affect patient compliance. High levels of total and LDL and low levels of HDL cholesterol are major risk factors for coronary atherosclerosis. Correcting lipid abnormalities can reduce the risk of development or progression of CHD. Diet and drugs are the main instruments available to normalize lipid levels. The choice of drug to combine with diet must be based on its specific effects on lipid metabolism, side effects, and efficacy in reducing CHD.

Language of Publication

English

Unique Identifier

98252199

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MeSH Heading (Major)

Coronary Disease|MO/*PC/PP; Hyperlipidemia|BL/DH/DT/*TH

MeSH Heading

Antilipemic Agents|AE/PD/TU; Cholesterol|BL; Combined Modality Therapy; Coronary Arteriosclerosis|ET/PC; Disease Progression; Human; Hydroxymethylglutaryl-CoA Reductase Inhibitors|TU; Lipids|ME; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Meta-Analysis; Multicenter Studies; Niacin|TU; Patient Compliance; Primary Prevention; Risk Factors; Survival Rate; Treatment Outcome

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0003-3197

Country of Publication

UNITED STATES

Record 5 from database: MEDLINE
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Title

Management of lipid disorders in the elderly.

Author

Playford DA; Watts GF

Address

University Department of Medicine, Royal Perth Hospital, Western Australia, Australia. daviplay@cyllene.uwa.edu.au

Source

Drugs Aging, 1997 Jun, 10:6, 444-62

Abstract

Cardiovascular disease has been inseparable from aging in developed societies and, as a result, it is the commonest cause of mortality in elderly populations. Atherosclerosis is associated with the progressive vascular accumulation of cholesterol-laden lipoproteins, and is linearly associated with the plasma level of low density lipoprotein (LDL) cholesterol. Clinical trials in patients aged < 65 years have conclusively shown that treatment of hypercholesterolaemia decreases the incidence of cardiovascular events and total mortality. However, few conclusive data are available regarding the treatment of hypercholesterolaemia in elderly patients. Extrapolation from clinical trials suggests that lipid lowering treatment in well selected elderly patients is effective in preventing cardiovascular events and is an efficient use of healthcare resources. In addition to cholesterol, high triglyceride and low high-density lipoprotein levels appear to be significant predictors of coronary artery disease in elderly patients. We do not advocate the indiscriminate screening of healthy elderly patients who have no other cardiovascular risk factors, because the marginal overall benefits are probably small and the costs of widespread screening and treatment high. On the other hand, chronological age itself cannot be considered a barrier to the screening and treatment of patients who have a good quality of life but have other cardiovascular risk factors and/or definite cardiovascular disease. Subgroup analysis of major clinical trials suggests that the aims of treatment should be to lower the LDL cholesterol level to 3.2 mmol/L (125 mg/dl), or the total cholesterol level to 5.2 mmol/L (200 mg/dl). Occasionally, multiple drug therapy is required to achieve this target, but statins (HMG-CoA reductase inhibitors) are the most commonly used first-line agents. With aggressive lowering of plasma lipid levels in this way, a reduction in clinical events is paralleled by regression of atheroma detectable by angiography, and an improvement in endothelial function. Global reduction of risk factors in elderly patients should always be undertaken, including dietary therapy, weight reduction in viscerally obese patients, postmenopausal estrogen replacement, smoking cessation, treatment of hypertension and control of diabetes mellitus. A secondary cause of dyslipidaemia should also be sought. The role of antioxidants is still not clear, but they are probably of little benefit in elderly patients. With the widespread use of effective, well tolerated treatments for lipid disorders in younger patients, significant improvements have already been attained in the morbidity and mortality associated with coronary artery disease. Since the current life expectancy at age 65 years is nearly 20 years in most Western countries, secondary prevention may increase the quality of life and the independent lifespan, even if eventual mortality is not delayed.

Language of Publication

English

Unique Identifier

97349993

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MeSH Heading (Major)

Aging|*BL/PH; Anticholesteremic Agents|*TU; Cardiovascular Diseases|EP/*PC; Hyperlipidemia|CL/DH/*DT/PP

MeSH Heading

Aged; Clinical Trials; Cost-Benefit Analysis; Diabetes Mellitus, Non-Insulin-Dependent|CO; Drug Therapy, Combination; Estrogens|DF; Female; Glucose Intolerance|CO; Human; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Lipoproteins, VLDL Cholesterol|BL; Male; Quality of Life; Risk Factors; Treatment Outcome

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

1170-229X

Country of Publication

NEW ZEALAND

Record 6 from database: MEDLINE
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Title

Butter, margarine and serum lipoproteins.

Author

Zock PL; Katan MB

Address

Department of Human Nutrition, Wageningen Agricultural University, The Netherlands.

Source

Atherosclerosis, 1997 May, 131:1, 7-16

Abstract

Intake of trans fatty acids unfavorably affects blood lipoproteins. As margarines are a major source of trans, claims for the advantages of margarines over butter need to be scrutinized. Here we review dietary trials that directly compared the effects of butter and margarine on blood lipids. We identified 20 studies in which subjects had stable body weights, and margarine and butter were exchanged in the diet at constant energy and fat intake. We calculated the changes in average blood lipid levels between study diets (49 comparisons) as a function of the percentage of calories as margarine substituted for butter. Replacing 10% of calories from butter by hard high-trans stick margarines lowered total serum cholesterol by 0.19, LDL by 0.11, and HDL by 0.02 mmol/l, and did not affect the total/HDL cholesterol ratio. Soft low-trans tub margarines decreased total cholesterol by 0.25 and LDL by 0.20 mmol/l, did not affect HDL, and decreased the total/HDL cholesterol ratio by 0.20. Based on the total/HDL cholesterol ratio, replacement of 30 g of butter per day by soft tub margarines would theoretically predict a reduction in coronary heart disease risk of 10%, while replacement of butter by hard, high-trans margarines would have no effect. Replacing butter by low-trans soft margarines favorably affects the blood lipoprotein profile and may reduce the predicted risk of coronary heart disease, but high-trans hard margarines probably confer no benefit over butter.

Language of Publication

English

Unique Identifier

97324043

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MeSH Heading (Major)

Butter|*; Dietary Fats|*AD; Lipoproteins|*BL; Margarine|*

MeSH Heading

Cholesterol|BL; Coronary Disease|PC; Human; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; MEDLINE; Support, Non-U.S. Gov't

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0021-9150

Country of Publication

IRELAND

Record 7 from database: MEDLINE
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Title

Dietary phytosterols as cholesterol-lowering agents in humans.

Author

Jones PJ; MacDougall DE; Ntanios F; Vanstone CA

Address

School of Dietetics and Human Nutrition, McGill University, MontrÆeal, QC, Canada.

Source

Can J Physiol Pharmacol, 1997 Mar, 75:3, 217-27

Abstract

Phytosterols (plant sterols), abundant in fat-soluble fractions of plants, are consumed at levels of 200-400 mg/day in Western diets. Chemically resembling cholesterol, phytosterols inhibit the absorption of cholesterol. Phytosterol consumption in human subjects under a wide range of study conditions has been shown to reduce plasma total and low density lipoprotein (LDL) cholesterol levels; however, the response varies widely. Greater cholesterol-lowering efficacy occurs with consumption of the saturated phytosterol sitostanol versus sitosterol or campesterol. Most studies report no effect of phytosterol administration in high density lipoprotein (HDL) cholesterol or triglyceride levels, although certain evidence exists for an HDL cholesterol raising effect of sitostanol. Phytosterol absorption is limited, although serum phytosterol levels have proven to be important indicators of both cholesterol absorption and synthesis. Serum phytosterols correlate with HDL cholesterol level. In addition, higher phytosterol/cholesterol ratios appear in HDL versus LDL particles, suggesting the existence of an intrinsic phytosterol action, in addition to the extrinsic effect on cholesterol absorption. In conclusion, addition to diet of the phytosterol sitostanol represents an effective means of improving circulating lipid profiles to reduce risk of coronary heart disease.

Language of Publication

English

Unique Identifier

97307514

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MeSH Heading (Major)

Anticholesteremic Agents|*AD/AE/ME; Cholesterol|AD/*BL/ME; Diet|*; Phytosterols|*AD/AE/ME

MeSH Heading

Human; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0008-4212

Country of Publication

CANADA

Record 8 from database: MEDLINE
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Title

Theoretical considerations of what regulates low-density-lipoprotein and high-density-lipoprotein cholesterol.

Author

Dietschy JM

Address

Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235-8887, USA.

Source

Am J Clin Nutr, 1997 May, 65:5 Suppl, 1581S-1589S

Abstract

The concentration of cholesterol carried in low-density-lipoprotein cholesterol (LDL-C) is predominantly dictated by metabolic events occurring in liver. LDL-C is derived from the intravascular metabolism of very-low-density lipoproteins, and, in every species, this lipoprotein particle is predominantly cleared by liver through receptor-dependent mechanisms. In addition to cholesterol absorbed from the diet, sterol is also synthesized within the body and this synthesis occurs predominantly in extrahepatic organs. When the amount of cholesterol input into the body is increased, there is expansion of the pools of sterol within liver cells and down-regulation of the receptors responsible for clearing LDL-C from the bloodstream. As a consequence, the concentration of LDL-C in plasma increases. When dietary cholesterol intake is kept constant, some long-chain saturated fatty acids further suppress hepatic LDL receptor activity whereas several unsaturated fatty acids have the opposite effect. These regulatory events are apparently articulated through the ability of these fatty acids to shift intracellular cholesterol between a regulatory and a storage pool. High-density lipoproteins, in contrast, function primarily to move excess cholesterol from the extrahepatic organs to liver for excretion. Although the concentration of high-density-lipoprotein cholesterol in the plasma may be influenced by the rate of apolipoprotein A-I production or the activity of cholesterol ester transfer protein, it is less clear whether dietary long-chain fatty acids have any effect on these processes. The regulatory effects of the saturated and unsaturated long-chain fatty acids on LDL-C concentrations can be shown in a variety of experimental animals and also in humans.

Language of Publication

English

Unique Identifier

97275728

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MeSH Heading (Major)

Lipoproteins, HDL Cholesterol|BL/*ME/PH; Lipoproteins, LDL Cholesterol|BL/*ME/PH; Liver|*ME; Models, Biological|*

MeSH Heading

Animal; Apolipoprotein A-I|ME; Cholesterol, Dietary|ME/PD; Fatty Acids|ME/PD; Human

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9165

Country of Publication

UNITED STATES

Record 9 from database: MEDLINE
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Title

Low-density lipoprotein removal methods by membranes and future perspectives.

Author

Matsuda Y; Malchesky PS; Nosé Y

Address

Department of Surgery, Baylor College of Medicine, Houston, Texas, USA.

Source

Artif Organs, 1996 Apr, 20:4, 346-54

Abstract

Since the application by Thompson et al. in 1975 of plasma exchange for the treatment of 2 patients with familial hyperlipidemia, plasma purification techniques for selective low-density lipoprotein (LDL) removal (i.e., LDL apheresis) have been developed and adopted for the management of this disease. Thermofiltration is one of the LDL apheresis systems that utilizes membrane techniques developed by Nose and Malchesky's group in 1985. This article reviews its rationale, in vitro studies, animal studies, and clinical investigation. Thermofiltration effectively and selectively removes LDL cholesterol while retaining in the plasma physiologically important macromolecules such as albumin and high-density lipoprotein (HDL) cholesterol. Based on the global view of the treatment of atherosclerosis by LDL apheresis, membrane techniques are as effective, safe, and simpler to apply than other methods. Additionally, these methods are effective for the removal of lipoprotein (a) and fibrinogen; thus, they can address the needs in these application areas.

Language of Publication

English

Unique Identifier

97013885

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MeSH Heading (Major)

Atherosclerosis|*TH; Lipoproteins, LDL Cholesterol|BL/*IP; Membranes, Artificial|*; Plasmapheresis|ST/*TD

MeSH Heading

Animal; Clinical Trials; Dextran Sulfate|CH/ME; Filtration; Heat; Heparin|PD; Human; Immunosorbents|CH/ME; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, VLDL Cholesterol|BL; Molecular Weight; Particle Size; Precipitation; Risk Factors

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0160-564X

Country of Publication

UNITED STATES

Record 10 from database: MEDLINE
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Title

The role of fiber in the treatment of hypercholesterolemia in children and adolescents.

Author

Kwiterovich PO Jr

Address

Department of Pediatrics, Johns Hopkins University, School of Medicine, Baltimore, MD, USA.

Source

Pediatrics, 1995 Nov, 96:5 Pt 2, 1005-9

Abstract

The effect of adding water-soluble fiber to a diet low in total fat, saturated fat, and cholesterol to treat hypercholesterolemic children and adolescents with elevated plasma low-density lipoprotein (LDL) cholesterol levels was assessed. In more than a half-dozen studies, the effect of water-soluble fiber on the LDL cholesterol level ranged from no change to as high as a 23% decrease using oat bran, psyllium, or locust bean gum. The wide range of effects in these studies may be related to the quality of the dietary intervention or to different methods of randomization, blinding, dietary assessment, and laboratory measurement. For example, the addition of supplemented soluble fiber (psyllium) to a step 1 diet may provide additional lowering of LDL cholesterol of 10% to 15%. However, in children consuming the more stringent step 2 diet, the addition of water-soluble fiber may have less additional effects on LDL cholesterol. As recommended by the National Cholesterol Education Program Expert Panel on Blood Cholesterol Levels in Children and Adolescents, dietary therapy, that is, a diet low in total fat, saturated fat, and cholesterol, remains the cornerstone of treatment for children and adolescents with elevated LDL cholesterol levels. The use of foods high in water-soluble fiber that contain no cholesterol and are low in saturated fat remains a good choice in children following a step 1 or step 2 diet. Additional clinical trials in larger numbers of well-defined subjects will be needed to assess further the utility of adding water-soluble fiber supplements to the National Cholesterol Education Program step 1 or step 2 diets.(ABSTRACT TRUNCATED AT 250 WORDS)

Language of Publication

English

Unique Identifier

96067496

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MeSH Heading (Major)

Dietary Fiber|*TU; Hypercholesterolemia|BL/*DH

MeSH Heading

Adolescence; Child; Cholesterol|BL; Cholesterol, Dietary|AD; Diet, Fat-Restricted; Human; Intervention Studies; Lipoproteins, LDL Cholesterol|BL; Nutrition Assessment; Oats; Polysaccharides|TU; Psyllium|TU; Randomized Controlled Trials; Solubility; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0031-4005

Country of Publication

UNITED STATES

Record 11 from database: MEDLINE
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Title

Monounsaturated oils do not all have the same effect on plasma cholesterol.

Author

Truswell AS; Choudhury N

Address

Human Nutrition Unit, University of Sydney, NSW, Australia.

Source

Eur J Clin Nutr, 1998 May, 52:5, 312-5

Abstract

Evidence assembled here indicates that when olive oil forms a major part of dietary fat in controlled human experiments, total and LDL-cholesterols are somewhat higher than when the same amount of fat is one of the modern predominantly monounsaturated oils: low erucic rapeseed or high oleic sunflower oil. Oils rich in monounsaturated fatty acids thus do not all have the same effect on plasma cholesterol. This phenomenon is explicable by consideration of the content of other fatty acids and the non-saponifiable fractions of the different monounsaturated oils. It helps to explain the discrepancy that has existed between the classic experiments (using olive oil), which found monounsaturated oils 'neutral', and some of the more recent experiments which found them more cholesterol-lowering than carbohydrates. Four published meta-analyses are reviewed. The three which included most of the published experiments show that monounsaturated fatty acids (MUFA) have less plasma cholesterol-lowering effect than polyunsaturated fatty acids.

Language of Publication

English

Unique Identifier

98292333

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MeSH Heading (Major)

Cholesterol|*BL; Dietary Fats, Unsaturated|*PD; Fatty Acids, Monounsaturated|AD/*PD

MeSH Heading

Erucic Acids|PD; Human; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Oleic Acid|PD; Plant Oils|PD

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0954-3007

Country of Publication

ENGLAND

Record 12 from database: MEDLINE
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Title

Management of dyslipidemia in adults.

Author

Ahmed SM; Clasen ME; Donnelly JE

Address

Wright State University School of Medicine, Dayton, Ohio, USA.

Source

Am Fam Physician, 1998 May, 57:9, 2192-2204, 2207-8

Abstract

The importance of treating dyslipidemias based on cardiovascular risk factors is highlighted by the National Cholesterol Education Program guidelines. The first step in evaluation is to exclude secondary causes of hyperlipidemia. Assessment of the patient's risk for coronary heart disease helps determine which treatment should be initiated and how often lipid analysis should be performed. For primary prevention of coronary heart disease, the treatment goal is to achieve a low-density lipoprotein (LDL) cholesterol level of less than 160 mg per dL (4.15 mmol per L) in patients with only one risk factor. The target LDL level in patients with two or more risk factors is 130 mg per dL (3.35 mmol per L) or less. For patients with documented coronary heart disease, the LDL cholesterol level should be reduced to less than 100 mg per dL (2.60 mmol per L). A step II diet, in which the total fat content is less than 30 percent of total calories and saturated fat is 8 to 10 percent of total calories, may help reduce LDL cholesterol levels to the target range in some patients. A high-fiber diet is also therapeutic. The most commonly used options for pharmacologic treatment of dyslipidemia include bile acid-binding resins, HMG-CoA reductase inhibitors, nicotinic acid and fibric acid derivatives. Other possibilities in selected cases are estrogen replacement therapy, plasmapheresis and even surgery in severe, refractory cases.

Language of Publication

English

Unique Identifier

98269154

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MeSH Heading (Major)

Antilipemic Agents|*TU; Cholesterol|*BL; Hyperlipidemia|BL/CL/CO/DH/DT/*TH

MeSH Heading

Adult; Coronary Disease|ET; Dietary Fats|AD; Dietary Fiber|AD; Drug Therapy, Combination; Human; Life Style; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Middle Age; Patient Education; Risk Factors; Teaching Materials

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-838X

Country of Publication

UNITED STATES

Record 13 from database: MEDLINE
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Title

Rationale for use of non-high-density lipoprotein cholesterol rather than low-density lipoprotein cholesterol as a tool for lipoprotein cholesterol screening and assessment of risk and therapy.

Author

Frost PH; Havel RJ

Address

Cardiovascular Research Institute and Department of Medicine, University of California, San Francisco 94143-0326, USA.

Source

Am J Cardiol, 1998 Feb, 81:4A, 26B-31B

Abstract

The plasma level of low-density lipoprotein (LDL) cholesterol is the "gold standard" for estimating the lipoprotein-related risk for complications of atherosclerotic vascular disease. LDL cholesterol concentrations are commonly estimated by the Friedewald formula that requires only the measurement (after overnight fasting) of plasma cholesterol and triglycerides along with high-density lipoprotein (HDL) cholesterol. This value, however, is not in fact a true estimate of LDL cholesterol but rather of LDL cholesterol along with variable, usually smaller, amounts of intermediate-density lipoprotein (IDL) cholesterol and lipoprotein(a). Estimation of LDL cholesterol levels by the Friedewald formula becomes progressively less accurate as plasma triglyceride concentrations increase, and the formula is generally considered inapplicable when triglyceride levels exceed 400 mg/dL. We believe that a very simple measurement-non-HDL cholesterol (serum cholesterol minus HDL cholesterol)-has considerable potential as a screening tool for identifying dyslipoproteinemias, for risk assessment, and for assessing the results of hypolipidemic therapy. Unlike the estimation of LDL cholesterol levels by the Friedewald formula, the estimation of non-HDL cholesterol concentrations requires no assumptions about the relation of very-low-density (VLDL) cholesterol levels to plasma triglyceride concentrations. This method includes all of the cholesterol present in lipoprotein particles now considered to be potentially atherogenic [VLDL, IDL, LDL, and lipoprotein(a)]. This article provides examples of the utility of non-HDL cholesterol concentrations in clinical medicine.

Language of Publication

English

Unique Identifier

98186005

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MeSH Heading (Major)

Atherosclerosis|*DI; Cholesterol|*BL; Coronary Disease|*BL; Lipoproteins|*BL; Lipoproteins, HDL Cholesterol|*BL; Lipoproteins, LDL Cholesterol|*BL

MeSH Heading

Apolipoproteins B|BL; Clinical Trials; Human; Lipids|BL; Lipoproteins, VLDL Cholesterol|BL; Risk Assessment; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.; Triglycerides|BL

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9149

Country of Publication

UNITED STATES

Record 14 from database: MEDLINE
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Title

Cholesterol intake and plasma cholesterol: an update.

Author

P2Namara DJ

Address

Egg Nutrition Center, Washington, DC 20006, USA.

Source

J Am Coll Nutr, 1997 Dec, 16:6, 530-4

Abstract

The misperception that dietary cholesterol determines blood cholesterol is held by many consumers in spite of evidence to the contrary. Many studies reported over the past 2 years have shown that dietary cholesterol is not a significant factor in an individual's plasma cholesterol level or cardiovascular disease (CVD) risk. Reports from the Lipid Research Clinics Research Prevalence Study and the Framingham Heart Study have shown that dietary cholesterol is not related to either blood cholesterol or heart disease deaths. In a similar manner, 10 clinical trials (1994 to 1996) of the effects of dietary cholesterol on blood lipids and lipoproteins indicate that addition of an egg or two a day to a low-fat diet has little if any effect on blood cholesterol levels. This observation was noted in young men and women with normal cholesterol levels as well as older subjects with elevated plasms cholesterol concentrations. The consistency of the clinical and the epidemiological data demonstrating that dietary cholesterol has little effect on plasma cholesterol in most individuals raises a number of questions regarding the justification of population wide restrictions on dietary cholesterol intake and egg consumption.

Language of Publication

English

Unique Identifier

98091915

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MeSH Heading (Major)

Cholesterol|*BL/ST; Cholesterol, Dietary|*AD/AE/ST

MeSH Heading

Cardiovascular Diseases|CI/PC; Clinical Trials; Female; Human; Male

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0731-5724

Country of Publication

UNITED STATES

Record 15 from database: MEDLINE
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Title

Effect of ursodeoxycholic acid on hepatic cholesterol metabolism.

Author

Einarsson K

Address

Dept. of Gastroenterology and Hepatology, Karolinska Institute, Huddinge University Hospital, Sweden.

Source

Scand J Gastroenterol Suppl, 1994, 204:, 19-23

Abstract

Oral administration of ursodeoxycholic acid (UDCA) renders bile unsaturated with cholesterol by reducing the hepatic output of cholesterol. Theoretically, several mechanisms may be of importance. In the present overview, the effect of treatment with UDCA on hepatic cholesterol metabolism is evaluated, in particular the influence on hepatic cholesterol synthesis, 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase activity, bile acid synthesis, 7 alpha-hydroxylation of cholesterol, and esterification of cholesterol--acyl coenzyme A: cholesterol acetyltransferase (ACAT) activity. It is apparent that UDCA treatment does not inhibit the hepatic HMG CoA reductase activity. Neither is ACAT activity or the cholesteryl ester content changed by UDCA. The catabolism of cholesterol to bile acids is unaffected or slightly increased during administration of UDCA. It is concluded that a stimulated degradation of cholesterol to bile acids may partly explain the decrease in hepatic secretion of cholesterol obtained during UDCA administration. It is suggested that the reduction in cholesterol absorption from the intestine seen during UDCA therapy may also be of importance.

Language of Publication

English

Unique Identifier

95125380

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MeSH Heading (Major)

Cholesterol|BI/*ME; Liver|*DE/EN/*ME; Ursodeoxycholic Acid|*PD/TU

MeSH Heading

Acyl Coenzyme A|BI/DE; Cholelithiasis|DT/ME; Cholesterol 7 alpha-Monooxygenase|BI/DE; Human; Hydroxymethylglutaryl CoA Reductases|BI/DE; Support, Non-U.S. Gov't

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0085-5928

Country of Publication

NORWAY

Record 16 from database: MEDLINE
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Title

Effect of long-chain fatty acids on low-density-lipoprotein-cholesterol metabolism.

Author

Woollett LA; Dietschy JM

Address

Department of Internal Medicine, University of Texas, Southwestern Medical Center at Dallas 75235-8887.

Source

Am J Clin Nutr, 1994 Dec, 60:6 Suppl, 991S-996S

Abstract

The concentration of cholesterol in the low-density-lipoprotein (LDL) fraction of plasma is one of the major risk factors for coronary heart disease. Steady-state concentrations of LDL cholesterol in the plasma are determined primarily by the production rate and the rate of removal of LDL cholesterol from the circulation by receptor-dependent transport. The magnitude of these two processes is affected by the type of fatty acid in the diet. Saturated fatty acids with 14 and 16 carbon atoms suppress receptor-dependent LDL-cholesterol transport into the liver, increase the LDL-cholesterol production rate, and raise the plasma LDL-cholesterol concentration. The 9-cis 18:1 fatty acid restores receptor activity, lowers the production rate, and decreases the plasma LDL-cholesterol concentration. In contrast with these fatty acids, the 18:0 and 9-trans 18:1 fatty acids are biologically inactive and so do not change the circulating LDL-cholesterol concentration.

Language of Publication

English

Unique Identifier

95067752

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MeSH Heading (Major)

Dietary Fats|*ME; Fatty Acids|*ME; Lipoproteins, LDL Cholesterol|*BL

MeSH Heading

Animal; Cholesterol Esters|AN; Cholesterol, Dietary|ME; Human; Liver|CH; Receptors, LDL|ME; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.; Triglycerides|ME

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9165

Country of Publication

UNITED STATES

Record 17 from database: MEDLINE
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Title

Defects in steroidogenic enzymes. Discrepancies between clinical steroid research and molecular biology results.

Author

Zachmann M

Address

Department of Pediatrics, University of Zurich, Kinderspital, Switzerland.

Source

J Steroid Biochem Mol Biol, 1995 Jun, 53:1-6, 159-64

Abstract

Molecular biology has clarified the understanding of steroidogenic enzyme genetics. Nevertheless, there are discrepancies between fundamental and clinical experience. (1) Why do patients with "pure" 17 alpha-hydroxylase or 17,20-desmolase deficiency exist, when one cytochrome regulates both steps? A case of interest is discussed, who had "pure" 17,20-desmolase deficiency until adolescence, but additional 17 alpha-hydroxylase deficiency thereafter. (2) In 11 beta-hydroxylase deficiency, it was puzzling to find 18-hydroxylated compounds, and, in isolated hypoaldosteronism, normal cortisol, since 11 beta- and 18-hydroxylation were thought to be regulated together. This has now been explained by differences in the fasciculata and glomerulosa. The occurrence of 11 beta-hydroxylase deficiency of 17-hydroxylated steroids only, however, remains enigmatic. (3) 3 beta-Hydroxysteroid dehydrogenase deficiency does not only seem to exist in classic (mutations of type II gene), but also in late-onset cases. In them, no molecular basis could be found. (4) Also, in cholesterol side-chain cleavage, there is an inequity: while evidently one cytochrome regulates 20- and 22-hydroxylation, pregnenolone is formed when 20 alpha OH-cholesterol, but not when cholesterol, is added to adrenal tissue of deficient patients. Other factors (promoters, fusion proteins, adrenodoxin, cAMP-dependent expression of genes, and/or proteases), or hormonal replacement in patients may be responsible for these discrepancies.

Language of Publication

English

Unique Identifier

95352443

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MeSH Heading (Major)

Steroid Hydroxylases|*DF/*GE; Steroids|*BI

MeSH Heading

Aldehyde-Lyases|DF/GE; Cholesterol|ME; Cholesterol Monooxygenase (Side-Chain-Cleaving)|DF/GE; Cytochrome P-450|DF/GE; Human; Steroid 17 alpha-Monooxygenase|DF/GE; Support, Non-U.S. Gov't

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0960-0760

Country of Publication

ENGLAND

Record 18 from database: MEDLINE
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Title

Extracorporeal removal of lipids by dextran sulfate cellulose adsorption.

Author

Olbricht CJ

Address

Department of Nephrology, Medical School Hannover, Germany.

Source

Artif Organs, 1996 Apr, 20:4, 332-5

Abstract

Extracorporeal removal of low-density lipoprotein (LDL) cholesterol by dextran sulfate adsorption is indicated in patients with diet and drug resistant hyper-cholesterolemia to prevent or to regress coronary heart disease. Plasma separation is the first step in the process, followed by adsorption of LDL cholesterol and lipoprotein (a) (Lp[a]) to negatively charged dextran sulfate covalently bound to cellulose beads. The reduction per treatment in LDL cholesterol is 65-75% and in Lp(a) 40-60%. In most patients one treatment per week is sufficient to reduce mean LDL to 100-150 mg/dl. Minor side effects occur in 2-6% of treatments. Major side effects are rare. In uncontrolled studies long-term treatment was associated with inhibition of progression and induction of regression of coronary artery disease. LDL apheresis by dextran sulfate may increase blood perfusion of some tissues, and preliminary results indicate a beneficial effect on therapy resistant nephrotic syndrome with hypercholesterolemia.

Language of Publication

English

Unique Identifier

97013881

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MeSH Heading (Major)

Hypercholesterolemia, Familial|*TH; Lipoproteins, LDL Cholesterol|BL/*IP; Plasmapheresis|*

MeSH Heading

Adsorption; Blood Proteins|IP/ME; Cellulose|CH/ME; Dextran Sulfate|CH/ME; Human; Lipoproteins, VLDL Cholesterol|BL/IP; Triglycerides|BL/IP

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0160-564X

Country of Publication

UNITED STATES

Record 19 from database: MEDLINE
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Title

Apolipoprotein E polymorphism and dietary plasma cholesterol response.

Author

Tikkanen M; Huttunen JK; Pajukanta PE; Pietinen P

Address

Department of Medicine, University of Helsinki, Finland.

Source

Can J Cardiol, 1995 Oct, 11 Suppl G:, 93G-96G

Abstract

All studies have demonstrated a strong association between plasma cholesterol and apoE phenotypes in the following order: E4/E4 > E4/E3 > E3/E3 > E3/E2. It has been thought possible that the apoE gene might be involved in the modulation of dietary plasma cholesterol responses, perhaps explaining the differences in cholesterol concentrations. Some dietary intervention studies have suggested that apoE4 individuals react to dietary change with exaggerated cholesterol responses. In one study, apoE4/E4 individuals responded by increased cholesterol reductions during low fat intake, and by increased cholesterol elevations during switchback to high fat diet. Plausible mechanisms have been postulated which could explain such differences. However, other studies have reported no differences in plasma lipid responses among apoE phenotypes. The studies cannot be directly compared because of different designs and study populations with differing apoE allele frequencies. Thus the possible role of genetic variation in the apoE gene in the modulation of dietary plasma lipid responses remains to be confirmed in prospective dietary studies, involving diets both rich and poor in fat and cholesterol.

Language of Publication

English

Unique Identifier

96062899

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MeSH Heading (Major)

Apolipoproteins E|*GE; Cholesterol, Dietary|*BL; Polymorphism (Genetics)|*; Variation (Genetics)|*

MeSH Heading

Human; Lipoproteins|BL; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Phenotype

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0828-282X

Country of Publication

CANADA

Record 20 from database: MEDLINE
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Title

Role of dietary fish protein in the regulation of plasma lipids.

Author

Jacques H; Gascon A; Bergeron N; Lavigne C; Hurley C; Deshaies Y; Moorjani S; Julien P

Address

DÆepartement de nutrition humaine et de consommation, UniversitÆe Laval, Ste-Foy, QuÆebec.

Source

Can J Cardiol, 1995 Oct, 11 Suppl G:, 63G-71G

Abstract

The following studies have been carried out to compare the effects of fish protein with other dietary proteins on plasma cholesterol and lipoproteins in animal models and in humans. In rabbits, fish protein has been shown to induce relatively variable effects compared to casein and soy protein on serum cholesterol depending in part on the origin of dietary lipids with which it is combined. In a protein-lipid interaction study, casein, soy or cod protein were combined with corn or coconut oil. Casein and soy protein in the presence of corn oil induced lower serum cholesterol levels despite its combination with either corn or coconut oil. This is in part due to serum high density lipoprotein (HDL) cholesterol concentrations, which were consistently higher with cod protein than with either casein or soy protein, regardless of the dietary lipid source. In rabbits, this rise in HDL cholesterol was associated with a decrease in very low density lipoprotein (VLDL) triglycerides and an increase in postheparin plasma lipoprotein lipase activity. The effects of lean white fish on plasma lipoproteins also have been investigated in post and premenopausal women fed a low-fat, high P/S (polyunsaturated/saturated fat) ratio diet. In postmenopausal women, lean white fish compared with other animal protein products induced higher concentrations of plasma cholesterol, LDL-apolipoprotein (apo) B and HDL cholesterol, mainly in the HDL3 fraction. In premenopausal women, lean white fish induced lower concentrations of VLDL triglycerides and higher concentrations of LDL-apoB in plasma.(ABSTRACT TRUNCATED AT 250 WORDS)

Language of Publication

English

Unique Identifier

96062895

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MeSH Heading (Major)

Cholesterol|*BL; Dietary Proteins|AN/ME/*PD; Lipoproteins|*BL; Seafood|*

MeSH Heading

Amino Acids|AN; Animal; Human; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, VLDL Cholesterol|BL; Support, Non-U.S. Gov't; Triglycerides|BL

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0828-282X

Country of Publication

CANADA

Record 21 from database: MEDLINE
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Title

What benefit can be derived from treating normocholesterolemic patients with coronary artery disease?

Author

Brown G; Stewart BF; Zhao XQ; Hillger LA; Poulin D; Albers JJ

Address

Department of Medicine, University of Washington School of Medicine, Seattle, USA.

Source

Am J Cardiol, 1995 Sep, 76:9, 93C-97C

Abstract

Controversy still remains regarding the possible clinical or arteriographic benefit of intensive lipid-altering therapy in patients who have coronary artery disease and apparently normal lipid levels. Resolution of this controversy appears to depend on an improved understanding of the role of variables other than total or low density lipoprotein cholesterol levels. A comparison of the "normolipidemic" subgroup of The Familial Atherosclerosis Treatment Study patients and The Harvard Atherosclerosis Reversibility Project patients indicates that low levels of high density lipoprotein cholesterol and elevated levels of apolipoprotein B appear to increase considerably the likelihood of benefit from intensive lipid-altering therapy. Other risk-related variables such as systolic blood pressure and lipoprotein(a) further contribute to the prediction of risk and possibly to the potential for treatment benefit.

Language of Publication

English

Unique Identifier

96016228

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MeSH Heading (Major)

Anticholesteremic Agents|*TU; Cholesterol|*BL; Coronary Disease|BL/*DT/RA

MeSH Heading

Adult; Apolipoproteins B|BL; Coronary Angiography; Human; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Middle Age; Randomized Controlled Trials; Risk Factors; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9149

Country of Publication

UNITED STATES

Record 22 from database: MEDLINE
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Title

Range of serum cholesterol values in the population developing coronary artery disease.

Author

Kannel WB

Address

Department of Medicine, Evans Memorial Research Foundation, Boston University School of Medicine/Framingham Heart Study, Massachusetts, USA.

Source

Am J Cardiol, 1995 Sep, 76:9, 69C-77C

Abstract

Blood lipids have been established as fundamental to atherogenesis, and there is a better understanding of the pathogenesis of atherosclerosis and of the various pharmacologic agents available to counter the mechanisms involved. However, more optimal lipid levels must be established for treatment of both the healthy population and persons already with coronary artery disease (CAD). In the Framingham Study cohort, those with elevated serum total cholesterol (> 275 mg/dl) had an increased risk of adverse outcomes whether healthy or with CAD. Compared with persons with cholesterol levels < 200 mg/dl (< 5.17 mmol/liter), the risk ratios for patients with elevated cholesterol levels were 3.8 for reinfarction, 2.6 for CAD mortality, and 1.9 for overall mortality. The prevalence of cholesterol levels > or = 240 mg/dl (> or = 6.21 mmol/liter) in persons who had sustained myocardial infarction was 35-52% in men and 66% in women, but 20% of myocardial infarctions occurred in people who had cholesterol levels < 200 mg/dl (< 5.17 mmol/liter). The average levels of serum total cholesterol and low density lipoprotein (LDL) cholesterol (225 mg/dl [5.82 mmol/liter] and 150 mg/dl [3.88 mmol/liter], respectively) at which CAD events occurred in men were below the levels recommended for treatment according to the guidelines of the National Cholesterol Education Program. In women, these levels were only slightly above the guideline levels. The average cholesterol levels at which CAD events occurred were substantially higher in women and decreased with age. Also, a steady decline in the average cholesterol levels of patients over the decades reflected chiefly the aging of the cohort.(ABSTRACT TRUNCATED AT 250 WORDS)

Language of Publication

English

Unique Identifier

96016225

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MeSH Heading (Major)

Cholesterol|*BL; Coronary Disease|*BL/EP/PC

MeSH Heading

Adult; Aged; Anticholesteremic Agents|TU; Apolipoproteins B|BL; Female; Human; Hyperlipidemia|DT/EP; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Male; Middle Age; Prevalence; Sex Factors; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9149

Country of Publication

UNITED STATES

Record 23 from database: MEDLINE
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Title

Worldwide distribution of blood lipids and lipoproteins in childhood and adolescence: a review study.

Author

Brotons C; Ribera A; Perich RM; Abrodos D; Magana P; Pablo S; Terradas D; Fernández F; Permanyer G

Address

Cardiology Department, Hospital General Universitari Vall d'Hebron, Barcelona, Spain. brotons@ar.vhebron.es

Source

Atherosclerosis, 1998 Jul, 139:1, 1-9

Abstract

Review and pooled analysis of the relevant worldwide literature was investigated from 1975 to 1996. Eighteen surveys out of 54 were suitable for analysis according to the selection criteria. This represents a total of 60494 observations from 26 countries all over the world. Data suggests differences as great as 76 mg/dl when comparing northern European countries to black African children. The overall curve of cholesterol with age observed in the pooled population indicates a pre-adolescent peak and then a slightly inverse change is observed for both boys and girls, from 3 to 12 years old being almost coincident absolute values. Beyond age 12, values for boys continue to slightly decrease to age 16, while for girls values tend to increase through this age-range. The curve in the late teens (16-18 years) tends to reach pre-teen levels for both sexes, although girls have consistently higher absolute values than boys. There is a great variation in the specific age-sex and race levels of cholesterol among different populations or even in the same populations over a period of time. However, an apparently universal pattern of an early rise, a fall, and a subsequent rise in mean values of total cholesterol by age from the preadolescence to late teens is observed. More data are needed on total cholesterol and lipid fractions between late school age and mid-adulthood.

Language of Publication

English

Unique Identifier

98363466

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MeSH Heading (Major)

Lipids|*BL; Lipoproteins|*BL

MeSH Heading

Adolescence; Child; Child, Preschool; Cholesterol|BL; Female; Human; Lipoproteins, HDL Cholesterol|BL; Male; Racial Stocks; Reference Values; Triglycerides|BL; World Health Organization

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0021-9150

Country of Publication

IRELAND

CAS Registry/EC Number

0 (Lipids); 0 (Lipoproteins); 0 (Lipoproteins, HDL Cholesterol); 0 (Triglycerides); 57-88-5 (Cholesterol)

Record 24 from database: MEDLINE
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Title

Pharmacological control of phagocyte function: inhibition of cholesterol accumulation.

Author

Paoletti R; Bellosta S; Bernini F

Address

Institute of Pharmacological Sciences, University of Milan, Italy.

Source

Ann N Y Acad Sci, 1997 Dec 15, 832:, 322-9

Abstract

Phagocytes play a major role in several diseases. In particular mononuclear phagocyte-derived foam cells have a prominent role in the development of the atherosclerotic lesions. Macrophages are present in all stages of atherogenesis; they internalize lipoproteins and accumulate cholesterol. Moreover, lipid-filled macrophages, by secreting extracellular matrix-degrading enzymes, may weaken rupture-prone atherosclerotic plaques, thus increasing the probability of precipitating atherosclerotic acute symptoms (i.e., myocardial infarction, angina, etc.). Therefore, control of cellular functions and cholesterol accumulation in macrophages represent pharmacological targets against atherosclerosis. In our laboratory we studied the effect of calcium antagonists on cellular cholesterol esterification in cultured macrophages. We also demonstrated that the HMG-CoA reductase inhibitors (vastatins) fluvastatin and simvastatin prevented cholesterol deposition in cultured human and murine macrophage by inhibiting modified LDL endocytosis. Interestingly, vastatin activity was more pronounced in cholesterol-loaded macrophages (i.e., foam cells) than in normal cells. In conclusion, in vitro pharmacological control of cholesterol accumulation in macrophages may be achieved with some calcium antagonists and vastatins independently of their effects on blood pressure or cholesterolemia.

Language of Publication

English

Unique Identifier

98369683

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MeSH Heading (Major)

Cholesterol|*ME; Hydroxymethylglutaryl-CoA Reductase Inhibitors|*PD; Macrophages|DE/*PH; Phagocytes|DE/*PH

MeSH Heading

Animal; Cholesterol Esters|ME; Human; Macrophages, Peritoneal|DE/PH; Nifedipine|PD; Phagocytosis|DE; Progesterone|PD; Verapamil|PD

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0077-8923

Country of Publication

UNITED STATES

CAS Registry/EC Number

0 (Cholesterol Esters); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 21829-25-4 (Nifedipine); 52-53-9 (Verapamil); 57-83-0 (Progesterone); 57-88-5 (Cholesterol)

Record 25 from database: MEDLINE
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Title

Current thinking in lipid lowering.

Author

Ballantyne CM

Address

Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA.

Source

Am J Med, 1998 Jun 22, 104:6A, 33S-41S

Abstract

In addition to elevated low-density lipoprotein (LDL) cholesterol, which has been conclusively proven to play a critical role in atherogenesis and coronary artery disease (CAD), other lipoprotein abnormalities are associated with CAD, such as reduced high-density lipoprotein (HDL) cholesterol; increased triglyceride-rich lipoproteins (very low density and intermediate-density lipoproteins); increased lipoprotein(a); small, dense LDL; and LDL with increased susceptibility to oxidation. Other, nonlipid factors such as homocysteine, fibrinogen, C-reactive protein, and soluble cell adhesion molecules may also have a role in risk stratification. The present US treatment guidelines, which focus on LDL cholesterol, stratify risk assessment and intensity of treatment by the presence of CAD; therefore, noninvasive imaging techniques such as ultrafast computed tomography and positron-emission tomography (PET) of the heart, which enable early detection of CAD, are useful in risk assessment. Because the influence of risk factors depends on their severity and combination, global risk assessment provides a necessary guide to the appropriate intensity of treatment. Agents are available that reduce LDL cholesterol and triglyceride and increase HDL cholesterol; although lipoprotein(a), LDL particle size, LDL oxidation, and homocysteine can also be altered, the clinical effects of such alterations are not known. Combination therapy that simultaneously improves multiple components of the lipid profile may provide additional benefit compared with monotherapy. To provide cost-effective treatment to the most patients, high-risk patients must be identified through systematic screening. Then each patient should be treated with the most cost-effective agent(s) that will enable achievement of the lipid levels recommended in the guidelines.

Language of Publication

English

Unique Identifier

98347992

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MeSH Heading (Major)

Antilipemic Agents|*TU; Coronary Disease|BL/DT/*PC; Lipoproteins|*BL

MeSH Heading

Human; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Risk Assessment; Risk Factors; Triglycerides|BL

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9343

Country of Publication

UNITED STATES

CAS Registry/EC Number

0 (Antilipemic Agents); 0 (Lipoproteins); 0 (Lipoproteins, HDL Cholesterol); 0 (Lipoproteins, LDL Cholesterol); 0 (Triglycerides)

Record 26 from database: MEDLINE
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Title

Assessing the observed relationship between low cholesterol and violence-related mortality. Implications for suicide risk.

Author

Kaplan JR; Muldoon MF; Manuck SB; Mann JJ

Address

Comparative Medicine Clinical Research Center, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina 27157-1040, USA. kaplan@cpm.bgsm.edu

Source

Ann N Y Acad Sci, 1997 Dec, 836:, 57-80

Abstract

Health advocacy groups advise all Americans to restrict their dietary intake of saturated fat and cholesterol as an efficacious and safe way to lower plasma cholesterol concentrations and thus reduce the risk of coronary heart disease and other atherosclerotic disorders. However, accumulating evidence suggests that naturally low or clinically reduced cholesterol is associated with increased nonillness mortality (principally suicide and accidents). Other evidence suggests that such increases in suicide and traumatic death may be mediated by the adverse changes in behavior and mood that sometimes accompany low or reduced cholesterol. These observations provided the rationale for an ongoing series of studies in monkeys designed to explore the hypothesis that alterations in dietary or plasma cholesterol influence behavior and that such effects are potentiated by lipid-induced changes in brain chemistry. In fact, the investigations in monkeys reveal that reductions in plasma cholesterol increase the tendency to engage in impulsive or violent behavior through a mechanism involving central serotonergic activity. It is speculated that the cholesterol-serotonin-behavior association represents a mechanism evolved to increase hunting or competitive foraging behavior in the face of nutritional threats signaled by a decline in total serum cholesterol (TC). The epidemiological and experimental data could be interpreted as having two implications for public health: (1) low-cholesterol may be a marker for risk of suicide or traumatic death and (2) cholesterol lowering may have adverse effects for some individuals under some circumstances.

Language of Publication

English

Unique Identifier

98279766

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MeSH Heading (Major)

Cholesterol|BL/*PH; Serotonin|*PH; Suicide|*; Violence|*

MeSH Heading

Animal; Cholesterol, Dietary|AE; Dietary Fats|AE; Human; Meta-Analysis; Risk Factors

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0077-8923

Country of Publication

UNITED STATES

Record 27 from database: MEDLINE
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Title

Estrogen replacement therapy and cardiovascular protection: lipid mechanisms are the tip of an iceberg.

Author

Nasr A; Breckwoldt M

Address

Department of Obstetrics and Gynecology, University of Assiut, Egypt.

Source

Gynecol Endocrinol, 1998 Feb, 12:1, 43-59

Abstract

Cardiovascular disease remains a major cause of mortality among postmenopausal women. After menopause, atherogenesis is promoted by a number of metabolic and vascular changes. A multitude of observational clinical studies have come to the conclusion that estrogen replacement therapy (ERT) reduces cardiovascular risk by approximately 50% and that estrogen's favorable effects on the lipid profile can explain only 25-50% of the overall observed reduction. Estrogens are now known to have potent anti-atherogenic properties through lipid and non-lipid mechanisms; both will be highlighted in view of the recent literature. Estrogens induce favorable changes on lipids and lipoproteins, partly by increasing HDL-cholesterol and decreasing both LDL-cholesterol and lipoprotein (a). Non-lipid mechanisms of estrogen action include decreasing insulin resistance, serum fibrinogen, factor VII and plasminogen activator inhibitor-1 (PAI-1). Moreover, estrogens maintain endothelial cell integrity, decrease expression of adhesion molecules, lower systemic blood pressure, promote vasodilatation, decrease platelet aggregability, inhibit vascular smooth muscle cell proliferation, possess potent antioxidant and calcium antagonist activities, inhibit adrenergic responses and downregulate platelet and monocyte reactivity. Also mentioned are recent reports linking estrogen to the renin-angiotensin system, relaxin, serotonin and homocysteine. What was once thought of as a simple action is now being increasingly appreciated as a complex, multifaceted mechanism, which serves to prove that estrogen is a powerful cardiovascular agent.

Language of Publication

English

Unique Identifier

98187458

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MeSH Heading (Major)

Atherosclerosis|ET/*PC; Cardiovascular Diseases|*PC; Estrogen Replacement Therapy|*; Estrogens|*TU; Lipids|*ME/PH

MeSH Heading

Aged; Endothelium|CY/PH; Female; Hemostasis|PH; Human; Insulin|ME; Lipoproteins, HDL Cholesterol|ME; Lipoproteins, LDL Cholesterol|ME; Menopause; Middle Age; Muscle, Smooth, Vascular|PH; Somatropin|PH

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0951-3590

Country of Publication

ENGLAND

Record 28 from database: MEDLINE
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Title

Stable angina pectoris: recent advances in predicting prognosis and treatment.

Author

Willerson JT

Address

Texas Heart Institute, Houston, USA.

Source

Adv Intern Med, 1998, 43:, 175-202

Abstract

Substantial progress has been made in the ability to predict individuals at the highest risk of acute myocardial infarction and occlusive cerebrovascular events, as well as in the ability to reduce these risks by vigorous reductions in serum cholesterol and LDL cholesterol concentrations. The development of stents has been a clear advance in the interventional treatment of coronary heart disease in that stents provide an effective acute treatment for significant coronary narrowings in symptomatic patients and reduce the risk of restenosis lesions subsequently. Heparin-coated stents appear to provide additive protection against the risk of thrombosis and the future development of restenosis lesions. Preliminary studies done on human carotid atherosclerotic plaque suggest that unstable plaque might be detected in the future by their temperature heterogeneity, which helps identify plaques with relatively thin fibrous caps, marked inflammation, and adjacent lipid pools.

Language of Publication

English

Unique Identifier

98167082

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MeSH Heading (Major)

Angina Pectoris|BL/ET/PC/*TH; Coronary Disease|BL/ET/PC/*TH

MeSH Heading

Angioplasty, Transluminal, Percutaneous Coronary; Anticoagulants|AD; Antilipemic Agents|TU; Atherosclerosis|DI/PA/PP; Body Temperature; Carotid Artery Diseases|DI/PA/PP; Cerebrovascular Disorders|ET/PC; Cholesterol|BL; Coronary Artery Bypass; Coronary Thrombosis|PC; Disease Progression; Forecasting; Heparin|AD; Human; Lipids|AN; Lipoproteins, LDL Cholesterol|BL; Myocardial Infarction|ET/PC; Prognosis; Recurrence; Risk Factors; Stents

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0065-2822

Country of Publication

UNITED STATES

Record 29 from database: MEDLINE
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Title

Comparison of efficacy and cost among lipid-lowering agents in patients with primary hypercholesterolemia [see comments]

Author

Lacour A; Derderian F; LeLorier J

Address

Centre de recherche, Centre hospitalier de l'UniversitÆe de MontrÆeal, HÈotel-Dieu, QuÆebec.

Source

Can J Cardiol, 1998 Mar, 14:3, 355-61

Abstract

OBJECTIVE: To compare efficacy and cost of lipid-lowering agents in patients with primary hypercholesterolemia. DESIGN: A meta-analysis was conducted to determine estimates of efficacy for lipid-lowering agents. Efficacy was defined as the change in the ratio of total cholesterol:high density lipoprotein (HDL) induced by treatment. This ratio was selected because of its good predictive value for the risk of coronary disease. Lipid-lowering agents were grouped into three categories according to the decrease in the total cholesterol:HDL ratio. Acquisition prices for drugs were obtained from the Quebec provincial drug formulary. An analysis determined which drugs in each category 'purchased' the greatest decrease in ratio for the lowest cost. SETTING: Clinical trial study centres. PATIENTS: The population analyzed had a mean baseline total cholesterol:HDL ratio of 7.3, an average age of 50.5 years and mean proportion of men of 62.5%. INTERVENTIONS: Twelve lipid-lowering therapies at various doses were investigated. RESULTS: Drugs that were more recently introduced had the greatest effect on the total cholesterol:HDL ratio. A direct dose-effect relationship was not evident, although there was a trend in this direction. In each of the three categories, there was wide range of cost, suggesting that the same effect is available at a broad range of prices. The drugs with the greatest effect on the ratio at the lowest cost were fluvastatin 60 mg/day, fenofibrate (micronized) 200 mg/day and simvastatin 20 mg/day. CONCLUSION: These results can be useful for clinicians in the selection of agents that achieve a specified goal of therapy at the lowest cost.

Language of Publication

English

Unique Identifier

98212386

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MeSH Heading (Major)

Anticholesteremic Agents|AD/*TU; Hypercholesterolemia|*DT

MeSH Heading

Coronary Disease|PC; Dose-Response Relationship, Drug; Human; Lipoproteins, HDL Cholesterol|AN; Lipoproteins, LDL Cholesterol|AN; Male; Middle Age; Risk Factors; Support, Non-U.S. Gov't

Publication Type

CLINICAL TRIAL; CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL; REVIEW; REVIEW, TUTORIAL

ISSN

0828-282X

Country of Publication

CANADA

Record 30 from database: MEDLINE
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Title

Human granulosa cells use high density lipoprotein cholesterol for steroidogenesis.

Author

Azhar S; Tsai L; Medicherla S; Chandrasekher Y; Giudice L; Reaven E

Address

Geriatric Research, Education, and Clinical Center, Veterans Administration Palo Alto Health Care System, California 94304, USA.

Source

J Clin Endocrinol Metab, 1998 Mar, 83:3, 983-91

Abstract

This study examines the ability of human high density lipoproteins (HDL3) to deliver cholesteryl esters to human granulosa cells and describes the selective cholesterol pathway by which this occurs. Luteinized cells obtained from subjects undergoing in vitro fertilization-embryo transfer procedures were incubated with native HDL3 (or radiolabeled or fluorescently labeled HDL cholesteryl esters) to determine whether cells from humans (in which HDL is not the primary circulating lipoprotein species) can nevertheless interiorize and appropriately process cholesteryl esters for steroidogenesis. The results indicate that hormone-stimulated granulosa cells actively and efficiently use human HDL-derived cholesterol for progesterone production. More than 95% of the mass of HDL cholesteryl esters entering cells does so through the nonlysosomal (selective) pathway, i.e. cholesteryl esters released from HDL are taken up directly by the cells without internalization of apoproteins. Once internalized, the cholesteryl esters are either hydrolyzed and directly used for steroidogenesis or stored in the cells as cholesteryl esters until needed. The utilization of the internalized cholesteryl esters is a hormone-regulated event; i.e. luteinized human granulosa cells internalize and store large quantities of HDL-donated cholesteryl esters when available, but further processing of the cholesteryl esters (hydrolysis, re-esterification, or use in steroidogenesis) does not occur unless the cells are further stimulated to increase progesterone secretion.

Language of Publication

English

Unique Identifier

98165604

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MeSH Heading (Major)

Granulosa Cells|*ME/PH; Lipoproteins, HDL Cholesterol|*ME; Progesterone|*BI

MeSH Heading

Boron Compounds|PK; Cholesterol Esters|ME/PK; Cyclic AMP|PD; Female; Fluorescent Dyes|PK; Human; Lipoproteins|PD; Support, U.S. Gov't, Non-P.H.S.; Support, U.S. Gov't, P.H.S.; Time Factors

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0021-972X

Country of Publication

UNITED STATES

Record 31 from database: MEDLINE
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Title

Long-term efficacy and safety of fenofibrate and a statin in the treatment of combined hyperlipidemia.

Author

Ellen RL; McPherson R

Address

Department of Medicine, University of Ottawa Heart Institute, Canada.

Source

Am J Cardiol, 1998 Feb, 81:4A, 60B-65B

Abstract

To assess the long-term efficacy and use of fenofibrate together with a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor ("statin") in the treatment of elevated levels of triglycerides and low-density lipoprotein (LDL) cholesterol, we conducted a study that compared a before- and after-case series. The study involved 80 patients with a diagnosis of combined hyperlipidemia and existing coronary artery disease (81% of patients) or outpatients with > or = 3 risk factors for coronary artery disease who had been receiving treatment at a tertiary care center. Fasting biochemical measures were obtained at baseline during monotherapy with a statin consisting of pravastatin 20 mg once daily or simvastatin 10 mg once daily (39 patients) or fenofibrate 300 mg once daily (41 patients), and during a 2-year period of combination therapy. This combination therapy comprised fenofibrate 300 mg once daily or micronized fenofibrate 200 mg once daily taken together with pravastatin 20 mg once daily (63 patients) or simvastatin 10 mg once daily (17 patients). The main outcome measures were: (1) absolute and percent change in total cholesterol, triglycerides, LDL cholesterol, and high-density lipoprotein (HDL) cholesterol; (2) percentage of patients with alanine aminotransferase > or = 2x the upper limits of normal on any occasion; (3) percentage of patients with creatinine kinase > or = 3 times the upper limits of normal on any occasion; (4) absolute changes in alanine aminotransferase and creatinine phosphokinase; and (5) months on combination therapy. Patients receiving combination therapy had a mean total cholesterol (+/- standard error of the mean [SEM]) that was significantly decreased by 26+/-1%, triglycerides by 41+/-3%, and LDL cholesterol by 28+/-2%, and mean HDL cholesterol that was significantly increased by 22+/-6%. These changes correspond to mean absolute changes of total cholesterol: -75+/-5 mg/dL; triglycerides: -94+/-13 mg/dL; LDL cholesterol: -52+/-5 mg/dL; and HDL cholesterol: 5+/-1 mg/dL. During combination treatment, alanine aminotransferase increased by 2+/-2 U/liter (not significant) and creatinine phosphokinase decreased by 4+/-13 U/liter (not significant). During treatment, 8 patients (10%) had transitory isolated elevations in alanine aminotransferase levels > or = 2 times the upper limits of normal and 2 patients (2.5%) had an isolated and transitory elevation of creatinine kinase (> or = 3x but < 6x upper limits of normal) without associated muscle symptoms. Patient-years on combination therapy equaled 220.6 (average 2.06 years per patient). The results demonstrated that combination treatment with fenofibrate and low-dose simvastatin or pravastatin is generally safe and effective for the treatment of combined hyperlipidemia in patients with normal hepatic and renal function.

Language of Publication

English

Unique Identifier

98186011

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MeSH Heading (Major)

Antilipemic Agents|*AD; Hydroxymethylglutaryl-CoA Reductase Inhibitors|*AD; Hyperlipidemia, Familial Combined|*DT; Pravastatin|*AD; Procetofen|*AD; Simvastatin|*AD

MeSH Heading

Coronary Disease|ET; Female; Human; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Male; Middle Age; Risk Factors; Triglycerides|BL

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9149

Country of Publication

UNITED STATES

Record 32 from database: MEDLINE
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Title

Use of niacin, statins, and resins in patients with combined hyperlipidemia.

Author

Brown BG; Zambon A; Poulin D; Rocha A; Maher VM; Davis JW; Albers JJ; Brunzell JD

Address

Department of Medicine, University of Washington School of Medicine, Seattle 98195, USA.

Source

Am J Cardiol, 1998 Feb, 81:4A, 52B-59B

Abstract

Patients in the original Familial Atherosclerosis Treatment Study (FATS) cohort were subgrouped into those with triglyceride levels < or = 120 mg/dL (n = 26) and those with triglyceride levels > or = 190 mg/dL (n = 40). Their therapeutic responses to niacin plus colestipol, lovastatin plus colestipol, colestipol alone, or placebo were determined. Therapeutic response was also determined in the same 2 triglyceride subgroups (n = 12 and n = 27, respectively) of patients selected for low levels of high-density lipoprotein (HDL) cholesterol and coronary artery disease. These triglyceride criteria were chosen to identify patient subgroups with high likelihood of "pattern A" (normal-size low-density lipoprotein [LDL] particles and triglyceride < or = 120 mg/dL) or "pattern B" (small dense LDL and triglyceride > or = 190 mg/dL). Our findings in these small patient subgroups are consistent with the emerging understanding that coronary artery disease patients presenting with high triglyceride levels have lower HDL-C, smaller less buoyant LDL-C, and greater very low-density lipoprotein (VLDL) cholesterol and VLDL apolipoprotein B, and are more responsive to therapy as assessed by an increase in HDL-C and reduction in triglycerides, VLDL-C, and VLDL apolipoprotein B. In the FATS high-triglyceride subgroup with these characteristics, a tendency toward greater therapeutic improvement in coronary stenosis severity was observed among those treated with either of the 2 forms of intensive cholesterol-lowering therapy. This improvement is associated with therapeutic reduction of LDL-C and elevation of HDL-C, but also appears to be associated with drug-induced improvement in LDL buoyancy.

Language of Publication

English

Unique Identifier

98186010

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MeSH Heading (Major)

Anticholesteremic Agents|*AD; Antilipemic Agents|*AD; Colestipol|*AD; Hyperlipidemia, Familial Combined|BL/*DT; Lovastatin|*AD; Niacin|*AD

MeSH Heading

Apolipoproteins|BL; Clinical Trials; Cohort Studies; Coronary Disease|ET; Drug Therapy, Combination; Human; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Risk Factors; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.; Triglycerides|BL

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9149

Country of Publication

UNITED STATES

Record 33 from database: MEDLINE
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Title

Treatment of diabetic dyslipidemia.

Author

Garg A

Address

Center for Human Nutrition and the Department of Clinical Nutrition, University of Texas Southwestern Medical Center at Dallas, and the Department of Veterans Affairs Medical Center, 75235-9052, USA.

Source

Am J Cardiol, 1998 Feb, 81:4A, 47B-51B

Abstract

Patients with diabetes mellitus have an increased risk for coronary artery disease due to hyperglycemia, hypertension, dyslipidemia, and other risk factors. The diabetic dyslipidemia in these patients is characterized by moderately high levels of (1) serum cholesterol and triglycerides; (2) small, dense low-density lipoprotein (LDL) particles; and (3) low high-density lipoprotein (HDL) cho-lesterol concentrations. Recent clinical trials have demonstrated the benefits of cholesterol-lowering therapy in both diabetic and nondiabetic patients, thus supporting aggressive treatment of diabetic dyslipidemia for coronary artery disease prevention. A 3-step approach is recommended for the treatment of diabetic dyslipidemia. First, modification of diet and lifestyle, including decreased intakes of cholesterol, cholesterol-raising fats, and total energy, and increased physical activity should be advised. Second, good glycemic control should be achieved with diet and hypoglycemic drugs, if needed. Third, lipid-lowering drugs should be used, if necessary. Non-HDL cholesterol levels, which include both very-low-density lipoprotein (VLDL) and LDL cholesterol, should be the target of cholesterol-lowering therapy. The use of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (the "statins") has become the first-line drug therapy for diabetic dyslipidemia. Bile acid sequestrants are effective cholesterol-lowering agents in normotriglyceridemic patients with non-insulin-dependent diabetes mellitus (NIDDM). Patients with severe hypertriglyceridemia may require fibric acids or n-3 polyunsaturated fatty acids. Nicotinic acid worsens hyperglycemia; therefore, it should be avoided in most cases. The efficacy and safety of estrogen-replacement therapy in postmenopausal women with diabetes needs to be determined. The combination of two lipid-lowering agents may be appropriate for some NIDDM patients but should be used judiciously.

Language of Publication

English

Unique Identifier

98186009

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MeSH Heading (Major)

Antilipemic Agents|*TU; Diabetes Mellitus, Non-Insulin-Dependent|CO/*TH; Diet|*; Hyperlipidemia|CO/*TH; Simvastatin|*TU

MeSH Heading

Cholesterol, Dietary|AD; Clinical Trials; Combined Modality Therapy; Coronary Disease|PC; Dietary Fats|AD; Estrogen Replacement Therapy|AE; Exercise; Female; Human; Life Style; Lipoproteins, LDL Cholesterol|BL; Lipoproteins, VLDL|BL; Postmenopause; Risk Factors; Support, Non-U.S. Gov't; Support, U.S. Gov't, Non-P.H.S.; Support, U.S. Gov't, P.H.S.; Weight Gain; 5,8,11,14,17-Eicosapentaenoic Acid|AD

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9149

Country of Publication

UNITED STATES

Record 34 from database: MEDLINE
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Title

Role of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors ("statins") in familial combined hyperlipidemia.

Author

Schonfeld G; Aguilar Salina C; Elias N

Address

Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110-1093, USA.

Source

Am J Cardiol, 1998 Feb, 81:4A, 43B-46B

Abstract

Familial combined hyperlipidemia (FCHL) is a heterogeneous genetic disorder characterized by multiple lipoprotein phenotypes. The genetic defect is unknown, although linkage to the region of the apolipoprotein (apo) A-I-apoC-III-apo A-IV gene cluster on chromosome 11 has been suggested. The metabolic abnormality in many affected individuals is overproduction of apoB-containing lipoproteins causing elevated levels of plasma cholesterol, triglycerides, or both. Low levels of high-density lipoprotein (HDL) cholesterol and an abundance of dense low-density lipoprotein (LDL) particles are other features contributing to the high association of this disorder with premature coronary artery disease. Many affected individuals need drug therapy to lower their lipid levels. The hepatic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or "statins," offer a potent therapeutic option in patients with FCHL. These drugs significantly decrease levels of total cholesterol, LDL cholesterol, and apoB, although their effects on HDL cholesterol and triglycerides are limited. The mechanisms by which statins exert their beneficial effects in patients with FCHL remain controversial. We studied 7 patients with FCHL and 5 genetically uncharacterized patients with mixed lipemia during treatment with pravastatin 20 mg/day. Metabolic parameters of very-low-density lipoprotein (VLDL)-apoB and LDL-apoB were studied using endogenous labeling with stable isotopes. In all patients pravastatin caused an increase in fractional catabolic rates of LDL-apoB without a significant effect on the production rates of apoB-containing lipoproteins. We cannot exclude the possibility that higher doses of statins may decrease VLDL and LDL production.

Language of Publication

English

Unique Identifier

98186008

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MeSH Heading (Major)

Antilipemic Agents|AD/*TU; Hydroxymethylglutaryl-CoA Reductase Inhibitors|AD/*TU; Hyperlipidemia, Familial Combined|*DT/GE/ME

MeSH Heading

Animal; Apolipoproteins|BL; Apolipoproteins B|ME; Apolipoproteins C|GE; Human; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Lipoproteins, VLDL|ME; Multigene Family

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9149

Country of Publication

UNITED STATES

Record 35 from database: MEDLINE
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Title

Effect of statins on metabolism of apo-B-containing lipoproteins in hypertriglyceridemic men.

Author

Vega GL; Grundy SM

Address

Center for Human Nutrition and Department of Clinical Nutrition, University of Texas Southwestern Medical Center at Dallas and the Veterans Affairs Medical Center at Dallas, 75235-9052, USA.

Source

Am J Cardiol, 1998 Feb, 81:4A, 36B-42B

Abstract

Our investigations indicate that most patients with moderate hypertriglyceridemia have marked defects in the metabolism of low-density lipoprotein (LDL) apolipoprotein B. Moreover, these patients have 2 major defects in the metabolism of triglyceride-rich lipoproteins, i.e., an accumulation of remnant lipoproteins (due in part to delayed hepatic clearance) and increased fractional conversion of very-low-density lipoprotein (VLDL) to LDL. Defective triglyceride-rich lipoprotein metabolism has been associated with insulin resistance. Statin therapy in hypertriglyceridemic patients improves the lipoprotein profile by decreasing both LDL cholesterol and remnant lipoproteins. However, statin therapy does not normalize LDL apolipoprotein B metabolism, and high-density lipoprotein (HDL) cholesterol levels remain low. Therefore, consideration may be given to combining a statin with a drug that alters triglyceride metabolism (e.g., fibrate or nicotinic acid) in high-risk patients with hypertriglyceridemia.

Language of Publication

English

Unique Identifier

98186007

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MeSH Heading (Major)

Antilipemic Agents|*TU; Apolipoproteins B|*ME; Hydroxymethylglutaryl-CoA Reductase Inhibitors|*TU; Hypertriglyceridemia|DT/*ME; Lipoproteins, LDL|*ME; Lovastatin|*TU

MeSH Heading

Comparative Study; Gemfibrozil|TU; Human; Insulin Resistance; Lipoproteins|BL; Lipoproteins, LDL Cholesterol|BL; Lipoproteins, VLDL Cholesterol|BL; Male; Niacin|TU

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9149

Country of Publication

UNITED STATES

Record 36 from database: MEDLINE
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Title

Hypertriglyceridemia, atherogenic dyslipidemia, and the metabolic syndrome.

Author

Grundy SM

Address

Department of Clinical Nutrition, Center for Human Nutrition, University of Texas Southwestern Medical Center at Dallas, 75235-9052, USA.

Source

Am J Cardiol, 1998 Feb, 81:4A, 18B-25B

Abstract

The importance of high serum cholesterol, especially a high level of low-density lipoprotein (LDL) cholesterol, as a risk factor for coronary artery disease is well established. Likewise, efficacy for decreasing risk for coronary artery disease by LDL-lowering therapy has recently been documented through clinical trials. However, many high-risk patients manifest elevated serum triglyceride levels, and the role of hypertriglyceridemia in causation of coronary artery disease remains to be elucidated. Nonetheless, there is growing evidence that hypertriglyceridemia is a marker for increased risk for coronary artery disease; in fact, it can serve as a marker for several atherogenic factors. These factors include increased concentrations of atherogenic triglyceride-rich lipoproteins; the atherogenic lipoprotein phenotype, or lipid triad; and the metabolic syndrome. The lipid triad consists of elevated serum triglycerides, small LDL particles, and low high-density lipoprotein (HDL) cholesterol. The metabolic syndrome includes the coexistence of the lipid triad, elevated blood pressure, insulin resistance (plus glucose intolerance), and a prothrombotic state. Many previous studies indicate that hypertriglyceridemia is strongly associated with all of these atherogenic factors. The clinical approach to treatment of patients with hypertriglyceridemia thus requires a broad-based strategy that includes reduction of atherogenic triglyceride-rich lipoproteins, reversal of the lipid triad, and favorable modification of the metabolic syndrome. The development of therapeutic regimens to effect these changes poses a challenge for future research on the problem of hypertriglyceridemia.

Language of Publication

English

Unique Identifier

98186004

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MeSH Heading (Major)

Atherosclerosis|*ME; Hyperlipidemia|*ME; Hypertriglyceridemia|DT/EP/GE/*ME

MeSH Heading

Animal; Antilipemic Agents|TU; Coronary Disease|ET; Human; Hydroxymethylglutaryl-CoA Reductase Inhibitors|TU; Hypertension|CO; Insulin Resistance; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL|BL; Lipoproteins, LDL Cholesterol|BL; Lipoproteins, VLDL|BL; Multivariate Analysis; Risk Assessment; Risk Factors; Syndrome; Triglycerides|BL

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9149

Country of Publication

UNITED STATES

Record 37 from database: MEDLINE
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Title

Recent advances in elucidating Niemann-Pick C disease.

Author

Vanier MT; Suzuki K

Address

INSERM Unit 189, Lyon-Sud Medical School, Oullins, France. vanier@univ-lyon1.fr

Source

Brain Pathol, 1998 Jan, 8:1, 163-74

Abstract

Lysosomal sequestration of endocytosed LDL-derived cholesterol, premature and abnormal enrichment of cholesterol in trans Golgi cisternae and accompanying anomalies in intracellular sterol trafficking are the hallmark phenotypic features of the Niemann-Pick C (NPC) lesion. A variable severity of these alterations has been observed, with only partial correlation between clinical and biochemical phenotypes. NPC also affects the metabolism of sphingolipids, and other biochemical abnormalities have been reported. Occurrence of neurofibrillary tangles in the brain of patients with a slowly progressive course is a recent intriguing observation. Genetic heterogeneity was established by cell hybridization and linkage studies. The two complementation groups could not be distinguished from each other by clinical, cellular or biochemical criteria, suggesting that the two gene products may interact or function sequentially. The major (> 90% of patients) NPC1 gene was mapped to 18q11 and recently isolated by positional cloning. The cDNA sequence predicts a 1278-amino acid protein, with 13 to 16 possible transmembrane regions and a putative cholesterol-sensing domain. Two murine models of the disease involving the same gene are known. The murine cDNA and the npc(nih) mutation have been characterized. Described homologies of the NPC1 protein are in line with its putative involvement in cellular cholesterol traffic.

Language of Publication

English

Unique Identifier

98117378

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MeSH Heading (Major)

Niemann-Pick Disease|GE/ME/*PA

MeSH Heading

Cholesterol|ME; Endocytosis|PH; Genetic Heterogeneity; Human; Lipids|ME; Lipoproteins, LDL Cholesterol|ME; Lysosomes|PA; Phenotype

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

1015-6305

Country of Publication

SWITZERLAND

Record 38 from database: MEDLINE
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Title

Dietary saturated and trans fatty acids and lipoprotein metabolism.

Author

Mensink RP; Temme EH; Hornstra G

Address

Department of Human Biology, Limburg University, Maastricht, The Netherlands.

Source

Ann Med, 1994 Dec, 26:6, 461-4

Abstract

Earlier studies have shown that not all saturated fatty acids are equally hypercholesterolaemic: stearic acid (C18:0) and saturated fatty acids with less than 12 carbon atoms are thought not to raise serum cholesterol levels. This suggests that the cholesterol-raising effects of saturated fatty acids can be attributed to lauric acid (C12:0), myristic acid (C14:0) and palmitic acid (C16:0). These three saturated fatty acids also have different effects on serum total cholesterol levels. Results from recent controlled dietary experiments suggest that lauric acid raises serum total and low-density lipoprotein (LDL) cholesterol levels slightly less, and myristic acid more, as compared with palmitic acid. Myristic acid, however, also causes higher levels of high-density lipoprotein (HDL) cholesterol. Stearic acid has only a slight effect on serum LDL and HDL cholesterol levels as compared with oleic acid. Trans monounsaturated fatty acids, however, increase LDL and decrease HDL cholesterol levels. Precise effects on lipoproteins of short and medium chain triglycerides (C4:0-C10:0) have never been examined.

Language of Publication

English

Unique Identifier

95209831

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MeSH Heading (Major)

Fatty Acids, Monounsaturated|*AE; Hypercholesterolemia|*ET; Lauric Acids|*AE; Lipoproteins|*ME; Myristic Acids|*AE; Palmitic Acids|*AE

MeSH Heading

Human; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Support, Non-U.S. Gov't

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0785-3890

Country of Publication

ENGLAND

Record 39 from database: MEDLINE
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Title

Overview of amphotericin B colloidal dispersion (amphocil).

Author

Stevens DA

Address

Department of Medicine, Santa Clara Valley Medical Center, San Jose, California 95128-2699.

Source

J Infect, 1994 May, 28 Suppl 1:, 45-9

Abstract

Amphotericin B colloidal dispersion (ABCD) is an equimolar mixture of amphotericin B and cholesteryl sulphate with desirable preparation and stability characteristics. It allows the intravenous delivery of amphotericin B in doses up to 7 mg/kg daily. Peak serum concentrations of amphotericin B, given as ABCD, are lower, AUC0-infinity similar and half-life longer than deoxycholate amphotericin B. In vitro activity may be altered with respect to the deoxycholate preparation, some isolates being more resistant and others more susceptible. Preclinical toxicology with ABCD revealed a safety factor of five to 19-fold compared with deoxycholate amphotericin B. Animal models of coccidioidomycosis, disseminated cryptococcosis, candidiasis and invasive aspergillosis indicated a better therapeutic ratio, especially in cryptococcosis. Phase I/II studies in humans demonstrate efficacy against coccidioidomycosis, candidiasis and aspergillosis at doses from 1-7 mg/kg/day in at least 100 patients. Renal toxicity was acceptable but infusion-related side effects and anaemia were common. Side effects appear to decrease on therapy. Comparative studies with deoxycholate amphotericin B are needed.

Language of Publication

English

Unique Identifier

94358456

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MeSH Heading (Major)

Amphotericin B|*AA/AD/PK/TU; Antiprotozoal Agents|*/AD/PK/TU; Cholesterol Esters|*/AD/PK/TU

MeSH Heading

Animal; Comparative Study; Half-Life; Human; Injections, Intravenous

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0163-4453

Country of Publication

ENGLAND

Record 40 from database: MEDLINE
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Title

Lipid profile during hormone replacement therapy: effect of different progestins?

Author

Campagnoli C; Belforte P; Di Sario MM; Lesca L

Address

Servizio di Ginecologia Endocrinologica, Ospedale Ginecologico Sant'Anna, Torino, Italy.

Source

Zentralbl Gynakol, 1997, 119 Suppl 2:, 1-6

Abstract

Oral estrogens cause a decrease of low density lipoprotein cholesterol (LDL-chol.) and, especially an increase of high density lipoprotein cholesterol (HDL-chol.) levels, which both have potentially favorable effects; they also cause a triglyceride level increase, which probably has no clinical relevance except in cases with basal hypertriglyceridemia. Transdermal estradiol causes generally a minor decrease in LDL-chol. and minor increase HDL-chol. levels, with no increase or even decrease in triglyceride levels. The addition of androgenic progestins at conventionally used doses, while not interfering with LDL-chol. variations, causes a HDL-chol. decrease, which contrasts the effect of oral estrogens and completely reverses the effect of transdermal estradiol. On the contrary, the addition of a non androgenic progestin does not interfere with any of the estrogen induced lipid profile modifications.

Language of Publication

English

Unique Identifier

98027325

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MeSH Heading (Major)

Estrogen Replacement Therapy|*; Lipids|*BL; Progestational Hormones, Synthetic|AD/*AE

MeSH Heading

Climacteric|BL/DE; Female; Human; Lipoprotein(a)|BL; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Triglycerides|BL

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0044-4197

Country of Publication

GERMANY

Record 41 from database: MEDLINE
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Title

Postmenopausal hormone replacement therapy and cardiovascular risk reduction. A review.

Author

Kafonek SD

Address

Division of Lipid Research Atherosclerosis Unit, Johns Hopkins University School of Medicine, Baltimore, Maryland.

Source

Drugs, 1994, 47 Suppl 2:, 16-24

Abstract

Administration of unopposed postmenopausal estrogen therapy protects against coronary heart disease (CHD) in women. This is mediated, in part, through beneficial effects on lipid and lipoprotein metabolism. Fewer data are available with regard to CHD risk reduction when a progesterone is required in addition to estrogen. Administration of continuous, rather than cyclic, estrogen-progesterone therapy may maintain the beneficial effects of estrogen and yet protect against the increase in endometrial cancer observed with estrogen therapy alone. Clinical guidelines for hormone replacement therapy await the completion of adequate controlled clinical trials.

Language of Publication

English

Unique Identifier

94298543

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MeSH Heading (Major)

Coronary Disease|*PC; Estrogen Replacement Therapy|*

MeSH Heading

Coronary Angiography; Drug Therapy, Combination; Estrogens|TU; Female; Human; Lipoproteins|ME; Lipoproteins, HDL Cholesterol|ME; Lipoproteins, LDL Cholesterol|ME; Progesterone|TU; Risk Factors; Triglycerides|ME

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0012-6667

Country of Publication

NEW ZEALAND

Record 42 from database: MEDLINE
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Title

Gene activation, apolipoprotein A-I/high density lipoprotein, atherosclerosis prevention and longevity.

Author

Luoma PV

Address

Regional Institute of Occupational Health in Oulu, Finland.

Source

Pharmacol Toxicol, 1997 Aug, 81:2, 57-64

Abstract

Recent studies in man and human apolipoprotein A-I transgenic animals emphasize the significance of apolipoprotein A-I and high density lipoprotein in antiatherogenesis. Several drugs and other compounds, e.g. phenobarbital, gemfibrozil, fenofibrate, prednisone, estrogen and alcohol, induce apolipoprotein A-I synthesis. They commonly produce serum lipoprotein patterns typical of a low risk of coronary heart disease, and many of them have been found to prevent atherogenesis, reduce coronary heart disease mortality and increase survival. These compounds act against atherosclerosis by using one or several mechanisms that include overexpression of the apolipoprotein A-I gene with an increase in serum apolipoprotein A-I and high density lipoprotein and promotion of reverse cholesterol transport, upregulation of the low density lipoprotein receptor gene with a decrease in serum apolipoprotein B and low density lipoprotein, maintenance of endothelial cell function and protection against thrombosis. They have been found to raise high density lipoprotein cholesterol and apolipoprotein A-I together with a decrease in cholesterol ester transfer protein activity, and to induce hepatic cholesterol 7 alpha-hydroxylase and cholesterol and bile acid elimination from the body. By raising the activities of apolipoprotein A-I/high density lipoprotein-associated paraoxonase and other antioxidative enzymes, the inducers have the capacity to prevent atherogenesis in arterial walls through inhibition of the oxidative modification of low density lipoprotein. Other antiatherogenic vascular actions of high density lipoprotein include interference with low density lipoprotein aggregation and uptake by endothelial cells, and competition with low density lipoprotein for endothelial-localized low density lipoprotein receptors. Apolipoprotein A-I/high density lipoprotein beneficially enhances fibrinolysis, decreases platelet aggregation, increases prostacyclin production and stabilization and prevents atherogenic immune and inflammatory responses. This gene activation or microsomal induction can prevent atherosclerosis and is a basis for tailoring effective new agents and optimal non-invasive therapy against atherosclerotic vascular disease to promote health and enhance longevity.

Language of Publication

English

Unique Identifier

97443725

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MeSH Heading (Major)

Apolipoprotein A-I|*BL/GE; Atherosclerosis|*GE/MO/*PC; Gene Expression|*/DE; Lipoproteins, HDL|*BL/GE

MeSH Heading

Animal; Antilipemic Agents|TU; Cholesterol|BL; Cholesterol Esters|BL; Diet; Human; Longevity; Male; Risk Factors

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0901-9928

Country of Publication

DENMARK

Record 43 from database: MEDLINE
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Title

Mechanisms of postprandial hyperlipidaemia--remnants and coronary artery disease.

Author

Karpe F

Address

King Gustaf V Research Institute, Department of Medicine, Karolinska Hospital, Stockholm, Sweden.

Source

Diabet Med, 1997 Aug, 14 Suppl 3:, S60-6

Abstract

High plasma concentrations of triglyceride-rich lipoprotein are associated with an increased risk of coronary artery disease (CAD). In the postprandial state, there is a large increase in chylomicron and very low-density lipoprotein (VLDL) concentrations. The accumulation of potentially atherogenic particles is controlled by the balance of their synthesis and clearance. Chylomicrons are rich in triglyceride and secreted by the intestine postprandially. Chylomicrons compete with VLDL for hydrolysis by lipoprotein lipase (LPL). This competition may cause the increase in large plasma concentration of VLDL seen in the postprandial state. Postprandial increases in atherogenic plasma lipoprotein concentrations are accentuated in insulin-resistant states. Insulin resistance is associated with greater flux of free fatty acids, which may in turn lead to enhanced synthesis of VLDL. Alimentary lipidaemia has been shown to effect changes in the coagulation cascade which may provide additional connections between postprandial lipaemia and CAD. Thus, specific postprandial changes in plasma lipids may be indicative of atherogenic risk. Measurement of postprandial plasma triglyceride concentration and the apo B-48 and apo B-100 contents in triglyceride-rich lipoprotein fractions are probably useful indicators of postprandial dyslipidaemia, but prospective studies of how these lipid variables relate to CAD progression are needed.

Language of Publication

English

Unique Identifier

97417243

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MeSH Heading (Major)

Chylomicrons|*ME; Coronary Disease|*ET; Hyperlipidemia|*CO/ME; Lipoproteins, VLDL|CL/*ME; Postprandial Period|*PH

MeSH Heading

Blood Coagulation|PH; Cholesterol Esters|ME; Cholesterol, Dietary|ME; Comparative Study; Human; Insulin Resistance|PH

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0742-3071

Country of Publication

ENGLAND

Record 44 from database: MEDLINE
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Title

Efficacy of alpha-glucosidase inhibitors on lipids in NIDDM subjects with moderate hyperlipidaemia.

Author

Leonhardt W; Hanefeld M; Fischer S; Schulze J

Address

Department of Metabolic Diseases, Clinic of Internal Medicine, Medical Faculty of the Technical University, Dresden, Germany.

Source

Eur J Clin Invest, 1994 Aug, 24 Suppl 3:, 45-9

Abstract

This paper summarizes literature data concerning the action of acarbose, an alpha-glucosidase inhibitor, on the concentrations of plasma lipids. Clinical trials in which acarbose has been used in the treatment of non-insulin-dependent diabetics have sometimes shown that it reduces serum triglycerides while it has little or no effect on serum cholesterol levels. The results of a randomized double-blind placebo-controlled study lasting 24 weeks are discussed in more detail. Under the controlled conditions, the effects of acarbose treatment on fasting concentrations of cholesterol, HDL-cholesterol, and triglycerides did not reach statistical significance for the entire patient group. However, in the highest tertile of initial cholesterol concentrations acarbose treatment led to significant lowering of the cholesterol concentration and of the total-to-HDL-cholesterol ratio. The most important benefits of acarbose were observed after a test meal given on day 0 and on week 24 of treatment. The triglyceride increment 1 h postprandial was significantly lowered. This was associated by a significant decrease of the insulin increment. Reduction of hyperinsulinaemia appears to be the mechanism by which acarbose treatment can improve plasma lipid concentrations.

Language of Publication

English

Unique Identifier

95094877

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MeSH Heading (Major)

alpha-Glucosidases|*AI; Diabetes Mellitus, Non-Insulin-Dependent|BL/CO/*DT; Hyperlipidemia|*BL/CO; Hypoglycemic Agents|*TU; Lipids|*BL; Trisaccharides|*TU

MeSH Heading

Cholesterol|BL; Comparative Study; Controlled Clinical Trials; Human; Lipoproteins, HDL Cholesterol|BL; Placebos; Randomized Controlled Trials; Time Factors; Triglycerides|BL

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0014-2972

Country of Publication

ENGLAND

Record 45 from database: MEDLINE
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Title

High-oil compared with low-fat, high-carbohydrate diets in the prevention of ischemic heart disease.

Author

Katan MB

Address

Department of Human Nutrition, Wageningen Agricultural University, Netherlands.

Source

Am J Clin Nutr, 1997 Oct, 66:4 Suppl, 974S-979S

Abstract

Reducing the intake of saturated fatty acids reduces the risk of coronary disease. This paper reviews the merits of two types of diets reduced in saturated fat. Low-fat, high-carbohydrate diets lower plasma low-density lipoprotein (LDL) but also lower high-density lipoprotein (HDL) concentrations and raise plasma very-low-density lipoprotein. The predicted net effect on coronary risk is zero. Weight loss with low-fat diets is modest and insufficient to offset the fall in HDL. Evidence for other beneficial effects of low-fat diets in incomplete. In contrast, diets low in saturated fat but high in unsaturated oils improve the ratio of HDL to LDL in plasma and thus reduce the predicted coronary risk. Recommendations to reduce total fat intake are therefore too imprecise; guidelines should aim specifically at saturated and probably also at trans fatty acids, whereas recommendations for restriction of cis-unsaturated fatty acids are not supported by firm scientific evidence.

Language of Publication

English

Unique Identifier

97463875

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MeSH Heading (Major)

Cholesterol, Dietary|*AD; Diet, Fat-Restricted|*; Dietary Carbohydrates|*AD; Fatty Acids|*AD; Myocardial Ischemia|*PC

MeSH Heading

Animal; Cholesterol|BL/ME; Comparative Study; Female; Human; Lipoproteins|BL; Male; Nutrition Policy; Time Factors; Weight Loss|PH

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9165

Country of Publication

UNITED STATES

Record 46 from database: MEDLINE
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Title

Micronised fenofibrate: a review of its pharmacodynamic properties and clinical efficacy in the management of dyslipidaemia.

Author

Adkins JC; Faulds D

Address

Adis International Limited, Auckland, New Zealand. demail@adis.co.nz

Source

Drugs, 1997 Oct, 54:4, 615-33

Abstract

Micronised fenofibrate is a new formulation of the fibric acid derivative fenofibrate. It is indicated for the treatment of patients with type IIa, IIb, III or IV dyslipidaemia who have failed to respond to dietary control or other nonpharmacological interventions. Micronised fenofibrate has improved absorption characteristics compared with the standard preparation, allowing a lower daily dosage and once-daily administration. The lipid-modifying profile of micronised fenofibrate is characterised by a decrease in low density lipoprotein (LDL) and total cholesterol levels, a marked reduction in elevated plasma triglyceride levels and an increase in high density lipoprotein (HDL) cholesterol levels. Consistent with the standard formulation, which is administered as 300mg daily in divided doses, the micronised preparation has demonstrated efficacy in the treatment of type IIa, IIb and IV primary dyslipidaemias but at a lower daily dosage of 200mg once daily. Because of its significant triglyceride-lowering effect, micronised fenofibrate appears to be of greatest benefit in patients with hypertriglyceridaemia (with or without hypercholesterolaemia), including patients with type 2 (non-insulin-dependent) diabetes mellitus and dyslipidaemia. In the comparisons available, micronised fenofibrate 200mg once daily was of similar efficacy to or less effective than the HMG-CoA reductase inhibitors simvastatin 20mg daily and pravastatin 20mg daily at reducing LDL and total cholesterol levels. However micronised fenofibrate produced greater improvements in triglyceride and, generally, HDL cholesterol levels than both simvastatin and pravastatin. Data on the long term tolerability of micronised fenofibrate are limited. However, data from a large short term (3-month) study have indicated that gastrointestinal disorders are the most frequent adverse events associated with therapy. Elevations in serum transaminase and creatine phosphokinase levels have been reported rarely with micronised fenofibrate. In conclusion, available data suggest that the more convenient lower once-daily dosage of micronisedfeno fibrate retains the beneficial lipid-modifying effects of the standard formulation. Further studies are required to determine whether the lipid changes achieved with micronised fenofibrate result in a reduction in cardiovascular morbidity and mortality.

Language of Publication

English

Unique Identifier

97479883

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MeSH Heading (Major)

Antilipemic Agents|PD/*TU; Hydroxymethylglutaryl-CoA Reductase Inhibitors|PD/*TU; Hyperlipidemia|BL/CO/*DT; Procetofen|AE/PD/*TU

MeSH Heading

Cardiovascular Diseases|DT/MO; Cholesterol|BL; Clinical Trials; Comparative Study; Controlled Clinical Trials; Diabetes Mellitus|CO; Dose-Response Relationship, Drug; Drug Delivery Systems; Drug Tolerance; Human; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL|BL; Pravastatin|PD/TU; Simvastatin|PD/TU

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0012-6667

Country of Publication

NEW ZEALAND

Record 47 from database: MEDLINE
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Title

Lipid modifying agents: mechanisms of action and reduction of cardiovascular disease.

Author

Scott R

Address

Lipid and Diabetes Research Group, Christchurch Hospital, New Zealand.

Source

Clin Exp Pharmacol Physiol, 1997 May, 24:5, A26-8

Abstract

1. Recent studies (4S, CARE, WOSCOPS) with the HMG CoA reductase inhibitors have shown that reductions of total cholesterol and LDL cholesterol reduce the risk for a new fatal or non-fatal cardiac event by approximately 30-35%, providing LDL is decreased by 25-35%. 2. Preliminary data also suggest that achieved LDL levels around 3.2 mmol/L results in no greater reduction in new events than when LDL is lowered even further. 3. There is considerable debate, nonetheless, as to whether these reduction in cardiovascular events are entirely a consequence of LDL reduction or whether the lipid-modifying agents have effects on lipoprotein structure, endothelial cell function, clotting and haemorrheological pathways. 4. The study results achieved with statins have obscured the role of fibrates as useful agents for reducing cardiovascular disease. Fibrates have a different mode of action to stains by reducing triglyceride-rich lipoprotein precursors and favourably altering LDL and HDL composition. 5. The practising clinician needs to consider the lipoprotein phenotype and to choose whether the ideal treatment is stain alone, fibrate alone or perhaps a combination.

Language of Publication

English

Unique Identifier

97288861

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MeSH Heading (Major)

Anticholesteremic Agents|*TU; Antilipemic Agents|*TU; Cardiovascular Diseases|BL/*PC; Hydroxymethylglutaryl-CoA Reductase Inhibitors|*TU

MeSH Heading

Drug Therapy, Combination; Human; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Randomized Controlled Trials

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0305-1870

Country of Publication

AUSTRALIA

Record 48 from database: MEDLINE
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Title

The underlying molecular mechanism of apolipoprotein E polymorphism: relationships to lipid disorders, cardiovascular disease, and Alzheimer's disease.

Author

Contois JH; Anamani DE; Tsongalis GJ

Address

Department of Pathology and Laboratory Medicine, Hartford Hospital, Connecticut, USA.

Source

Clin Lab Med, 1996 Mar, 16:1, 105-23

Abstract

Apolipoprotein E (apo E) polymorphism has important clinical correlates, including disorders of lipoprotein metabolism and atherosclerosis. This article provides a detailed methodology for apo E genotyping and discusses the link between apo E genotype and type III hyperlipoproteinemia, coronary heart disease (CHD), stroke, and Alzheimer's disease (AD). Although apo E genotype appears to provide significant information concerning the genetic component of CHD and AD risk, more research is needed before genotyping can be recommended as a routine screening tool. The data so far, however, implicate apo E as a major component of the genetic basis of cardiovascular disease and AD.

Language of Publication

English

Unique Identifier

97021226

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MeSH Heading (Major)

Alzheimer Disease|*GE/ME; Apolipoproteins E|*PH; Coronary Arteriosclerosis|*GE/ME; Hyperlipidemia|*GE/ME; Polymorphism (Genetics)|*

MeSH Heading

Alleles; Base Sequence; Cholesterol|BL; Electrophoresis, Polyacrylamide Gel; Genotype; Human; Lipoproteins, HDL Cholesterol|BL; Molecular Sequence Data; Mutation; Phenotype; Polymorphism, Restriction Fragment Length; Triglycerides|BL

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0272-2712

Country of Publication

UNITED STATES

Record 49 from database: MEDLINE
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Title

Fluvastatin in combination with other lipid-lowering agents.

Author

Jokubaitis LA

Address

Cardiovascular Clinical Research, Sandoz Research Institute, East Hanover, NJ 07936, USA.

Source

Br J Clin Pract Suppl, 1996 Jan, 77A:, 28-32

Abstract

Fluvastatin, a new synthetic inhibitor of HMGCoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase, has been studied in several models to examine its effects when used in combination with other lipid-modifying agents such as derivatives of fibric acid (bezafibrate), resins (cholestyramine), and niacin. The combination of fluvastatin with bezafibrate has been studied in a double-blind trial involving patients with well-documented familial hypercholesterolaemia. Fluvastatin 40 mg/day, combined with either bezafibrate 400 mg/day or cholestyramine 8 g/day, resulted in reductions in levels of low-density lipoprotein cholesterol (LDL-C), these being indistinguishable between the groups; however, significantly greater increases in levels of high-density lipoprotein cholesterol (21.3%) and reductions in levels of triglycerides (25.1%) were seen with the fluvastatin-bezafibrate combination. No notable increases were seen in levels of serum creatine kinase, aspartate aminotransferase, or alanine aminotransferase, and no cases of myopathy were observed. In a study model that examined low-dose combinations of fluvastatin with cholestyramine, reductions in levels of LDL-C of 15.8% and 19.3% were seen with fluvastatin 10 mg and 20 mg, respectively. After an 8-week interval in which a daily dosage of cholestyramine 8 g was added, from baseline, reductions of 26.3% in the 10 mg fluvastatin-cholestyramine group and 31.2% in the 20 mg fluvastatin-cholestyramine group were observed, whereas the placebo-cholestyramine group displayed a reduction of 14.9%. Doubling the resin dosage to 16 g/day for the final 8 weeks of the study provided little additional benefit. Myotoxicity has been observed when lovastatin is coadministered with niacin, and so the combination of niacin with fluvastatin has also been studied to examine the possibility of this effect occurring. Patients were randomised to either fluvastatin 20 mg or placebo for 6 weeks, after which time open-label niacin was administered to all patients and titrated to a final dosage of 3 g/day. After 6 weeks, fluvastatin produced a 20.8% reduction in LDL-C levels from baseline. When combined with niacin, a 43.7% reduction was noted at the week 15 endpoint, against the 26.5% reduction seen with niacin monotherapy. The combination was well tolerated, with no reports of myopathy or of significant elevations in creatine kinase or liver transaminase levels. Combinations of fluvastatin with a variety of other agents have been shown to have significant effects on lipid profiles, with no evidence to date of clinically remarkable safety findings. Thus, the use of combination therapies may result in optimal management of patients with moderately severe hypercholesterolaemia and mixed dyslipidaemic profiles.

Language of Publication

English

Unique Identifier

96306615

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MeSH Heading (Major)

Anticholesteremic Agents|*TU; Antilipemic Agents|*TU; Fatty Acids, Monounsaturated|*TU; Hypercholesterolemia|BL/*DT; Indoles|*TU

MeSH Heading

Bezafibrate|TU; Cholestyramine|TU; Drug Therapy, Combination; Human; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Niacin|TU; Randomized Controlled Trials

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0262-8767

Country of Publication

ENGLAND

Record 50 from database: MEDLINE
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Title

Lipoprotein alterations and atherosclerosis in the elderly.

Author

Corti MC; Barbato GM; Baggio G

Address

Istituto di Medicina Interna, UniversitÄa di Padova, Italy. CORTIC@UX1.UNIPD.IT

Source

Curr Opin Lipidol, 1997 Aug, 8:4, 236-41

Abstract

Lipoproteins play a key role in the pathogenesis of atherosclerotic diseases. With increasing age, modifications in the metabolism, distribution and correlates of lipoprotein lipids have been described. Age associated changes in lipoproteins are determined by several genetic and environmental factors, but in elderly populations, an important role is also played by the presence of comorbid diseases and poor health. In older populations, the ability of lipoprotein levels to predict cardiovascular risk is controversial. When lipoprotein levels are measured at old age, secondary changes in total and high density lipoprotein-cholesterol levels may lead to misclassification and to underestimation of associations. When analyzing associations in older populations, it is therefore important to consider measures of disease burden and comorbidity. When these caveats are taken into account, evidence from observational studies in older persons confirms the association between lipoprotein lipids, cardiovascular and cerebrovascular disease. Among older patients with cardiovascular disease, intervention trials have demonstrated that lipid lowering drugs can significantly reduce total and coronary heart disease mortality. Unequivocal evidence that lipid-lowering drugs are beneficial in old and very old persons without pre-existing cardiovascular disease is still lacking. Results from primary and secondary intervention trials in older men and women are needed to provide conclusive guidelines.

Language of Publication

English

Unique Identifier

97397502

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MeSH Heading (Major)

Aged|*PH; Atherosclerosis|*ET/PC; Lipoproteins|*ME

MeSH Heading

Cerebrovascular Disorders|ET; Cholesterol|BL; Clinical Trials; Cross-Sectional Studies; Female; Human; Lipoprotein(a)|BL; Lipoproteins, HDL Cholesterol|BL; Longitudinal Studies; Male

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0957-9672

Country of Publication

UNITED STATES

Record 51 from database: MEDLINE
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Title

Cardioprotection by estrogens: mechanisms of action--the lipids.

Author

Samsioe G

Address

Department of Obstetrics and Gynecology, Lund University Hospital, Sweden.

Source

Int J Fertil Menopausal Stud, 1994, 39 Suppl 1:, 43-9

Abstract

Reductions of total and LDL-cholesterol and, to a lesser extent, increase in HDL are known to decrease cardiovascular disease (CVD) incidence. All oral estrogens are known to induce such changes in a dose-dependent manner at doses commonly used in ERT, somewhat more markedly for estradiol than for conjugated equine estrogens (CEE). Low-dose estriol used for urogenital discomfort is void of lipid effect. Transdermal estradiol induces similar reductions in the important LDL fraction, whereas HDL is less affected. Modified, especially oxidized, LDL is particularly atherogenic. Accumulating evidence suggests estrogen inhibits LDL oxidation in a process not counteracted by progestins. Elevated triglycerides are considered an important risk factor in women aged about 50. Oral estradiol and, especially, conjugated estrogens augment serum triglycerides, whereas estrogens with non-oral delivery systems rather reduce triglyceride concentrations. The clinical significance of pharmacologically induced changes in triglycerides remains to be clarified. Estrogen-induced changes in the serum lipid profile, however, account for no more than a third of the cardioprotective effect. Lipoprotein (a), another important indicator of CVD risk, is probably also reduced by the action of estrogens. Neither lipoprotein (a) nor oxidized LDL is measured by the routine serum lipid profile. At this time it is impossible to deduce the quantitative importance of changes in these two variables with respect to cardioprotection by estrogens.

Language of Publication

English

Unique Identifier

94258230

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MeSH Heading (Major)

Cardiovascular Diseases|BL/*PC; Estrogens|*TU; Lipids|*BL

MeSH Heading

Animal; Estrogen Replacement Therapy; Female; Human; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Male; Menopause; Triglycerides|BL

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

1069-3130

Country of Publication

UNITED STATES

Record 52 from database: MEDLINE
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Title

Common genetic determinants of dyslipidemia: the hypertriglyceridemia/low-high-density lipoprotein syndrome.

Author

Galton DJ

Address

Department of Human Metabolism and Genetics, St. Bartholomews Hospital, London, England.

Source

J Cardiovasc Pharmacol, 1995, 25 Suppl 4:, S35-40

Abstract

Allelic frequencies of polymorphic variants at the lipoprotein lipase gene locus on chromosome 8 have been measured in subjects with premature coronary heart disease and/or dyslipidemia. One of the polymorphic variants involves a termination codon in exon 9 at the position of serine 447, which produces a truncated protein. Michaelis constants and Vmax for triolein and chylomicrons appear identical for the variant and native enzymes. Another informative polymorphism is a Hind 111 restriction site in intron 8 that shows marked asymmetric allelic distribution in subjects with hypertriglyceridemia/low-high-density lipoprotein and in subjects with premature coronary heart disease. It is hoped that this marker may lead to the identification of an etiological mutation in its vicinity to account for these disease associations.

Language of Publication

English

Unique Identifier

97063346

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MeSH Heading (Major)

Coronary Disease|EN/ET/*GE; Hyperlipidemia|EN/ET/*GE; Lipoproteins, HDL Cholesterol|*BL; Lipoproteins, LDL Cholesterol|*BL

MeSH Heading

Alleles; Chromosomes, Human, Pair 8; Female; Human; Lipoprotein Lipase|GE; Male; Pedigree; Polymorphism (Genetics); Risk Factors; Support, Non-U.S. Gov't

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0160-2446

Country of Publication

UNITED STATES

Record 53 from database: MEDLINE
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Title

Human obesity: from lipid abnormalities to lipid oxidation.

Author

Van Gaal LF; Zhang A; Steijaert MM; De Leeuw IH

Address

University Hospital Antwerp/Laboratory of Endocrinology, Department of Endocrinology, Clinical Nutrition and Metabolism, Faculty of Medicine, Wilrijk, Belgium.

Source

Int J Obes Relat Metab Disord, 1995 Sep, 19 Suppl 3:, S21-6

Abstract

The obese state has been recognized to accentuate the known risk factors for atherosclerotic disease as dyslipidemia, hypertension, glucose intolerance and insulin resistance. Among other risk factors, obesity is characterized by a series of lipid disturbances, such as hypercholesterolemia, high fasting (and postprandial) triglyceride levels, low HDL cholesterol, high apolipoprotein B, high small dense lipoprotein particles and alterations of serum and tissue LPL-activity. Although obesity is associated with such cluster of lipid abnormalities, these factors do not explain the complete process of atherogenesis in the obese subject. Other risk factors belonging to the polymetabolic syndrome-cluster, insulin resistance, hypertension, fibrinogen, add substantial but not full explanation to the atherothrombotic process. Over the last decade, a series of excellent studies have provided the background for a more indepth mechanism of atherosclerosis; the role of lipid peroxidation in particular has been one of the focuses of this current research. There exists a lot of evidence suggesting a major role for oxidized LDL and VLDL particles in the pathogenesis of atherosclerosis. Although obesity is characterized by dyslipidemia, less is known about the oxidation capacity of lipoproteins in obese subjects. We measured the oxidizability in vitro in 21 premenopausal women and compared them to 18 age-matched controls. The oxidizability of the non-HDL fraction is evaluated by measuring the fluorescence and thiobarbituric acid reactive substances (TBARS: MDA nM/mg non-HDL) at different time intervals of incubation. TBARS formation increased linearly with the increase of lipids both in non-obese and obese subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Language of Publication

English

Unique Identifier

96079153

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MeSH Heading (Major)

Lipids|*ME; Obesity|*ME/PP

MeSH Heading

Apolipoproteins B|ME; Body Composition|PH; Female; Human; Hyperlipidemia|ME; Lipoproteins, HDL Cholesterol|ME; Lipoproteins, LDL Cholesterol|ME; Oxidation-Reduction; Thiobarbituric Acid Reactive Substances|ME; Triglycerides|ME

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

Country of Publication

ENGLAND

Record 54 from database: MEDLINE
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Title

Trans fatty acids, lipoproteins, and coronary risk.

Author

Zock PL; Katan MB

Address

Department of Human Nutrition, Wageningen Agricultural University, The Netherlands.

Source

Can J Physiol Pharmacol, 1997 Mar, 75:3, 211-6

Abstract

Most dietary fatty acids contain at least one double bond, which is usually in the cis configuration. However, biohydrogenation in the rumen of cows and sheep, or catalytic hydrogenation of vegetable oils in the food industries, will convert some of the cis double bonds to the trans configuration. Trans fatty acid intake in western Europe and North America probably ranges from 5 to 15 g/day. Major dietary sources are frying fats used in industrial food preparation, margarines, and other spreads. In the past, margarines contained up to 50% trans fatty acids; however, these are now being phased out. Trans fatty acids raise serum low density lipoprotein (LDL) cholesterol and lower high density lipoprotein (HDL) cholesterol in humans when substituted for cis unsaturated fatty acids in the diet. These effects may be mediated by the cholesteryl ester transfer protein. Trans fatty acids also increase lipoprotein (a) levels relative to other fatty acids. The effects of trans fatty acids on the risk profile for coronary heart disease are thus unfavorable, and labels of food products should state the trans fatty acid content.

Language of Publication

English

Unique Identifier

97307513

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MeSH Heading (Major)

Coronary Disease|BL/EP/*ET; Dietary Fats, Unsaturated|*AD/ME; Lipoproteins|*BL

MeSH Heading

Fatty Acids, Unsaturated|AD/ME; Human; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Risk Factors; Stereoisomerism; Support, Non-U.S. Gov't

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0008-4212

Country of Publication

CANADA

Record 55 from database: MEDLINE
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Title

Angiographic trials of lipid-lowering therapy: an update.

Author

Mancini GB

Address

Vancouver Hospital and Health Sciences Centre, British Columbia, Canada.

Source

Curr Opin Lipidol, 1995 Dec, 6:6, 379-85

Abstract

The value of specific LDL apheresis in drug-resistant cases of hyperlipidaemia is reviewed, as well as new data on the prevention of new lesion formation, efficacy of therapy based on initial lipid levels, and the consequences of lipid lowering in the angioplasty setting. Studies undertaken in the carotid and femoral bed are included, as is a brief discussion of the use of probucol as an adjunct to lipid-lowering therapy. These studies have emerged on a backdrop of data focused more on reduction of clinical events than on morphologic changes. Studies on the clinical impact of lipid-lowering therapy are included to provide a linkage between the rationale and conclusions of the angiographic trials with the emerging demonstration that cholesterol lowering does indeed reduce both cardiovascular and total mortality without inducing significant noncardiovascular morbidity or mortality.

Language of Publication

English

Unique Identifier

96356355

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MeSH Heading (Major)

Antilipemic Agents|*TU; Arteriosclerosis|*DT; Blood Component Removal|*; Coronary Arteriosclerosis|DT/MO/PC/*TH; Hyperlipidemia|*DT; Lipoproteins, LDL|*BL

MeSH Heading

Cholesterol|BL; Clinical Trials; Coronary Angiography; Disease Progression; Hormones|TU; Human; Lipoproteins, LDL Cholesterol|BL; Meta-Analysis; Recurrence

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0957-9672

Country of Publication

UNITED STATES

Record 56 from database: MEDLINE
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Title

Trials of lipid-lowering therapy in primary prevention of coronary heart disease.

Author

Jones PH

Address

Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.

Source

Curr Opin Lipidol, 1995 Dec, 6:6, 365-8

Abstract

The effectiveness of lipid-regulating therapy in the primary prevention of coronary heart disease requires further investigation. The only data available are from trials conducted before the advent of more potent lipid-regulating agents, but several large trials currently in progress are expected to provide valuable evidence about the role of lipid-regulating intervention in primary prevention.

Language of Publication

English

Unique Identifier

96356352

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MeSH Heading (Major)

Antilipemic Agents|PD/*TU; Coronary Disease|*PC; Hyperlipidemia|*DT

MeSH Heading

Antihypertensive Agents|TU; Cholesterol|BL; Clinical Trials; Coronary Arteriosclerosis|PC; Female; Human; Lipoproteins, LDL Cholesterol|BL; Male; Risk Factors

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0957-9672

Country of Publication

UNITED STATES

Record 57 from database: MEDLINE
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Title

Phenotypic and genetic heterogeneity in Niemann-Pick disease type C: current knowledge and practical implications.

Author

Vanier MT

Address

INSERM-CNRS, Unit 189, Lyon-Sud School of Medicine, Oullins, France.

Source

Wien Klin Wochenschr, 1997 Feb, 109:3, 68-73

Abstract

The eponym "Niemann-Pick disease" includes two metabolically distinct entities. Niemann-Pick type C (NPC) is characterized by unique abnormalities of intracellular transport of exogenous cholesterol with sequestration of unesterified cholesterol in lysosomes, while Niemann-Pick types A and B are acid sphingomyelinase deficiencies resulting from mutations in the gene coding for lysosomal sphingomyelinase. Current knowledge regarding abnormalities of cholesterol processing in cultured cells from NPC patients is reviewed. The wide spectrum of expression of the disease is outlined. Based on experience with more than 350 patients, the problems encountered in the author's laboratory in the diagnosis of patients are discussed, as well as the relatively poor correlation between clinical and biochemical phenotypes. Recent major developments are, furthermore, reviewed. Cell hybridization studies have established an intergenic heterogeneity within NPC, consisting of one major (90% of patients) and one minor complementation group. Both groups show a wide phenotypic heterogeneity. The major gene has been mapped to 18q11-12, while the minor gene has been excluded from this region of chromosome 18. The function of both genes is yet unknown.

Language of Publication

English

Unique Identifier

97213381

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MeSH Heading (Major)

Genotype|*; Niemann-Pick Disease|DI/*GE/PA; Phenotype|*

MeSH Heading

Cells, Cultured; Cholesterol|ME; Chromosome Mapping; Chromosomes, Human, Pair 18; Diagnosis, Differential; Heterozygote Detection; Human; Infant, Newborn; Support, Non-U.S. Gov't

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0043-5325

Country of Publication

AUSTRIA

Record 58 from database: MEDLINE
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Title

Trans fatty acids and their effects on lipoproteins in humans.

Author

Katan MB; Zock PL; Mensink RP

Address

Department of Human Nutrition, Agricultural University, Wageningen, The Netherlands.

Source

Annu Rev Nutr, 1995, 15:, 473-93

Abstract

Trans fatty acids raise plasma low-density lipoprotein (LDL) cholesterol levels in volunteers when exchanged for cis unsaturated fatty acids in the diet. In addition, trans fatty acids may lower high-density lipoprotein (HDL) cholesterol levels and raise triglyceride and lipoprotein(a) levels in plasma. Trans and cis unsaturated fatty acids are thus not equivalent, and diets aimed at reducing the risk of coronary heart disease should be low in both trans and saturated fatty acids.

Language of Publication

English

Unique Identifier

96138953

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MeSH Heading (Major)

Fatty Acids|*PD; Lipoproteins|*BL

MeSH Heading

Female; Human; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Male; Triglycerides|BL

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0199-9885

Country of Publication

UNITED STATES

Record 59 from database: MEDLINE
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Title

The importance of body fat distribution in early life.

Author

Freedman DS

Address

Division of Nutrition, Centers for Disease Control and Prevention, Atlanta, Georgia 30341-3724, USA.

Source

Am J Med Sci, 1995 Dec, 310 Suppl 1:, S72-6

Abstract

It is possible that many of the conflicting findings concerning obesity and cardiovascular disease may be the result of the heterogeneous nature of obesity, adn that only certain subgroups of the obese are at increased risk. Over the last several decades, much attention has focused on the distribution of body fat as an important characteristic in the metabolic and clinical alterations associated with obesity. Several studies have shown that a relative excess of adipose tissue in the upper body, abdominal region, or at various truncal sites is associated with an increased risk of disease; furthermore, these associations are independent of the general level of obesity. This article presents a brief historical overview of the idea of body fat distribution, the measurement techniques that have been used, and the complications associated with an adverse distribution of body fat distribution; particular emphasis is given to studies that have examined fat patterning in early life. Although most investigators recognize that body fat distribution is important in the development of cardiovascular disease, several questions remain.

Language of Publication

English

Unique Identifier

96101363

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MeSH Heading (Major)

Adipose Tissue|*AH; Cardiovascular Diseases|*ET; Obesity|*CO

MeSH Heading

Child; Female; Human; Lipoproteins, LDL Cholesterol|BL; Lipoproteins, VLDL Cholesterol|BL; Male; Skinfold Thickness

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9629

Country of Publication

UNITED STATES

Record 60 from database: MEDLINE
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Title

The management of cholesterol in coronary heart disease risk reduction.

Author

Woodhead GA

Address

Lahey Hitchcock Medical Center, Department of Cardiovascular Medicine, Burlington, Mass, USA.

Source

Nurse Pract, 1996 Sep, 21:9, 45, 48, 51-3

Abstract

Coronary heart disease remains the number one cause of death in the American population. The Framingham Heart Study and other epidemiologic studies have demonstrated a direct relationship between elevated total and low-density lipoprotein cholesterol in the development of cardiovascular disease. This article focuses on secondary prevention, demonstrating that decreased cholesterol has a wide range of benefits in patients with cardiovascular disease. Emphasis is placed on the Scandinavian Simvastatin Survival Study which reported a 30% reduction of total mortality in a population of 4,444 patients with coronary heart disease who were treated with an HMG-CoA reductase inhibitor. The National Cholesterol Education Program guidelines for cholesterol risk reduction are reviewed. The impact of the health care provider as related to adherence and medication is discussed. Outcome issues of cost-effectiveness and resource utilization relating to cholesterol reduction are emphasized.

Language of Publication

English

Unique Identifier

97039241

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MeSH Heading (Major)

Coronary Disease|*ET; Hypercholesterolemia|BL/*CO/*PC

MeSH Heading

Antilipemic Agents|TU; Cholesterol|BL; Health Status Indicators; Human; Lipoproteins, LDL Cholesterol|BL; Nurse Practitioners; Nursing Assessment; Risk Factors

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0361-1817

Country of Publication

UNITED STATES

Record 61 from database: MEDLINE
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Title

Hypoalphalipoproteinemia (low high density lipoprotein) as a risk factor for coronary heart disease.

Author

Vega GL; Grundy SM

Address

Department of Clinical Nutrition, University of Texas, Southwestern Medical Center, Dallas 75235, USA.

Source

Curr Opin Lipidol, 1996 Aug, 7:4, 209-16

Abstract

Low HDL levels are inversely related to risk for coronary heart disease. Several different mechanisms may account for this relationship. First, low HDL levels may be directly atherogenic; second, a low HDL often denotes high levels of other atherogenic lipoproteins (for example, remnants); and third, a low HDL frequently accompanies other coronary risk factors (for example, insulin resistance, diabetes, and raised blood pressure). This multiplicity of relationships probably explains the power of low HDL levels to predict acute coronary events.

Language of Publication

English

Unique Identifier

97037868

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MeSH Heading (Major)

Coronary Disease|*ET; Lipoproteins, HDL|*ME; Tangier Disease|*CO/PP

MeSH Heading

Animal; Apolipoprotein A-I|DF/GE; Biological Markers; Carrier Proteins|AN/GE; Cholesterol Esters|ME; Cohort Studies; Comparative Study; Haplorhini; Human; Hypertriglyceridemia|PP; Lipoprotein Lipase|AN/ME; Lipoproteins, HDL Cholesterol|AN; Male; Mice; Reference Values; Risk Factors

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0957-9672

Country of Publication

UNITED STATES

Record 62 from database: MEDLINE
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Title

Ethnic differences in stroke: black-white differences in the United States population. SECORDS Investigators. Southeastern Consortium on Racial Differences in Stroke.

Author

Gaines K; Burke G

Address

University of Tennessee Medical Units, Memphis 38103, USA.

Source

Neuroepidemiology, 1995, 14:5, 209-39

Abstract

The US Black (African-American) population has a higher stroke incidence and mortality than the US White population. This article reviews the English language literature relating to observed racial and ethnic differences in stroke mortality, incidence, and risk factors. In addition, Black-White differences in stroke subtype, pathophysiology, outcome, recurrence, and treatment are reviewed. The significance of these racial and ethnic differences and directions for future research are explored.

Language of Publication

English

Unique Identifier

96043105

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MeSH Heading (Major)

Blacks|*; Cerebrovascular Disorders|*EP/ET/PC; Whites|*

MeSH Heading

Adult; Age Factors; Aged; Caucasoid Race; Cohort Studies; Comparative Study; Diabetes Mellitus|CO/EP; Female; Human; Hypertension|CO/EP; Incidence; Lipoproteins|BL; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, VLDL Cholesterol|BL; Male; Middle Age; Negroid Race; Prevalence; Recurrence; Risk Factors; Triglycerides|BL; United States|EP

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0251-5350

Country of Publication

SWITZERLAND

Record 63 from database: MEDLINE
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Title

Estrogens, progestins and lipid metabolism.

Author

Tikkanen MJ

Address

Dept. of Medicine, Helsinki University Central Hospital, Finland.

Source

Maturitas, 1996 May, 23 Suppl:, S51-5

Abstract

OBJECTIVES: To review some aspects in the recent literature related to the effects of postmenopausal estrogen and progestin use on major plasma lipoprotein risk factors for coronary heart disease (CHD). METHODS: Collection of relevant information from medical journals, and by the use of Medline and Current Contents. RESULTS: The beneficial effects of estrogen (LDL cholesterol reduction and HDL cholesterol elevation) are well established. The effects on HDL are modified to different degrees by progestins, depending on the androgenic properties of the latter: the 'sex steroid sensitive' HDL2 subfraction is decreased by nortestosterone derived progestins with androgenic activity. Recently developed methodology employing stable isotopes has helped to clarify underlying mechanisms. Progestins alone, as well as estrogen-progestin combinations have been shown to reduce the plasma levels of Lp(a), another lipoprotein risk factor for CHD. According to one study, estrogen administered alone had a similar effect. CONCLUSIONS: The effects of hormone replacement therapies on lipid metabolism have been partly established and investigations on the underlying mechanisms are being published. This information will be useful for developing new replacement regimens with more protection against CHD and less adverse effects.

Language of Publication

English

Unique Identifier

97018524

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MeSH Heading (Major)

Coronary Disease|BL/*PC; Estrogen Replacement Therapy|*; Lipids|*BL; Progestational Hormones|*AD

MeSH Heading

Adult; Aged; Female; Human; Lipoprotein(a)|BL; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Middle Age

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0378-5122

Country of Publication

IRELAND

Record 64 from database: MEDLINE
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Title

Dietary cholesterol and the optimal diet for reducing risk of atherosclerosis.

Author

McNamara DJ

Address

Department of Nutritional Sciences, University of Arizona, Tucson 85721, USA.

Source

Can J Cardiol, 1995 Oct, 11 Suppl G:, 123G-126G

Abstract

The importance of dietary cholesterol in the incidence of hypercholesterolemia in the population remains a topic of scientific debate. Analysis of the results from over 30 years of cholesterol feeding studies (n = 128) in more than 2750 patients indicate that for the majority of individuals modest changes in dietary cholesterol have little if any effect on plasma lipoprotein cholesterol levels. Data demonstrate that on average a change in cholesterol intake of 100 mg/day results in a change in plasma total cholesterol of 0.07 mmol/L (2.5 mg/dL). The studies also show that the extent of response to dietary cholesterol is independent of the amount of dietary fat and of the baseline plasma cholesterol level. In contrast, the dose adjusted plasma cholesterol response to a dietary cholesterol challenge is affected by the type of dietary fat and the baseline dietary cholesterol intake. Based on these data a reduction in dietary cholesterol intake from 450 to 300 mg/day will, on average, lower plasma cholesterol levels by 0.10 mmol/L (3.7 mg/dL). This decrease is modest and highly variable due to significant interindividual heterogeneity of responses. It is estimated that one-third of the population is sensitive to dietary cholesterol whereas two-thirds are resistant to plasma cholesterol changes. In comparison, a 1% decrease in energy intake from saturated fat decreases plasma cholesterol 0.08 mmol/L (3 mg/dL). Consumption of products marketed as 'No cholesterol' with high total and saturated fat clearly does not contribute to the optimal diet for reducing plasma cholesterol levels of risk of atherosclerosis.

Language of Publication

English

Unique Identifier

96062905

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MeSH Heading (Major)

Cholesterol, Dietary|*AD/BL; Coronary Arteriosclerosis|BL/*DH/EP/*PC; Diet|*

MeSH Heading

Cholesterol|BL; Human; Risk Factors

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0828-282X

Country of Publication

CANADA

Record 65 from database: MEDLINE
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Title

Unresolved issues in early trials of cholesterol lowering.

Author

LaRosa JC

Address

Tulane University Medical Center, Office of the Chancellor, New Orleans, Louisiana 70112-2699, USA.

Source

Am J Cardiol, 1995 Sep, 76:9, 5C-9C

Abstract

A reexamination of early intervention trials in patients with coronary artery disease (CAD) shows that a pessimistic view of cholesterol reduction in such patients is inappropriate. In observational studies, individuals with documented coronary artery disease and elevated cholesterol levels fare worse than individuals with normal or low cholesterol levels. Early trials of cholesterol reduction in individuals with coronary artery disease succeeded in lowering total cholesterol levels by only 5-15%. Nevertheless, when reviewed in meta-analysis, these trials demonstrated borderline effects on total mortality, statistically significant benefits in terms of morbidity and mortality due to cardiovascular disease and CAD, and no increase in mortality from noncardiovascular causes. Substantially greater lowering of low density lipoprotein (LDL) levels was achieved in early regression studies. In these studies, examples of improvement were noted in individual coronary artery segments. What was not appreciated initially was the dramatic reduction in coronary events. Older secondary prevention trials did not definitively address the benefits of cholesterol reduction in individuals whose cholesterol levels were only modestly elevated (total cholesterol, 160-240 mg/dl [4.14-6.21 mmol/liter], and LDL cholesterol levels 100-160 mg/dl [2.59-4.14 mmol/liter]). Several other issues were not addressed in these early studies, including the effect of declines in triglyceride levels, increases in high density lipoprotein (HDL) levels, and the effects in women and individuals aged > 60 years. Even with these limitations, a comparison of meta-analyses of other medical interventions--i.e. beta blockade and aspirin therapy--indicates that declines in coronary mortality are in the same range as obtained in older studies with modest cholesterol reduction--i.e., 20-25%.(ABSTRACT TRUNCATED AT 250 WORDS)

Language of Publication

English

Unique Identifier

96016215

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MeSH Heading (Major)

Anticholesteremic Agents|*TU

MeSH Heading

Aged; Clinical Trials; Coronary Arteriosclerosis|ET; Coronary Disease|DT/ET; Female; Human; Hypercholesterolemia|BL/CO/DT; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Male; Middle Age

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9149

Country of Publication

UNITED STATES

Record 66 from database: MEDLINE
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Title

Extending the benefit of lipid-regulating therapy to primary prevention.

Author

Jones PH; Gotto AM Jr

Address

Baylor College of Medicine, Houston, Texas, USA.

Source

Am J Cardiol, 1995 Sep, 76:9, 118C-121C

Abstract

In recent years, a number of published secondary prevention trials have further strengthened the rationale for aggressive lipid-regulating therapy in patients with established coronary artery disease. However, the role of lipid-regulating therapy in primary prevention is less well characterized. Several large primary prevention trials, using a variety of interventions, are ongoing in different populations. These include the Air Force Coronary/Texas Atherosclerosis Prevention Study, the West of Scotland Coronary Prevention Study, the Women's Health Initiative, and the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial. These investigations will extend the results of earlier primary prevention trials and further characterize the rationale for intervention.

Language of Publication

English

Unique Identifier

96016232

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MeSH Heading (Major)

Coronary Disease|BL/*PC; Lipids|*BL; Primary Prevention|*

MeSH Heading

Aged; Anticholesteremic Agents|TU; Female; Human; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Lovastatin|TU; Male; Middle Age; Pravastatin|TU; Randomized Controlled Trials

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9149

Country of Publication

UNITED STATES

Record 67 from database: MEDLINE
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Title

Preventing and arresting coronary atherosclerosis.

Author

Roberts WC

Address

Baylor Cardiovascular Institute, Baylor University Medical Center, Dallas, TX 75246, USA.

Source

Am Heart J, 1995 Sep, 130:3 Pt 1, 580-600

Abstract

The good news about coronary atherosclerosis is that it takes an awful lot of plaque before symptoms of myocardial ischemia occur. The bad news is that despite the need for large quantities of plaque for symptoms to occur, nevertheless nearly half of us in the United States eventually have the necessary quantity. Atherosclerosis is infrequently hereditary in origin. Most of us get atherosclerosis because we consume too much fat, cholesterol, and calories. The consequence is an elevated ( > 150 mg/dl) serum total cholesterol level, and the higher the number is above 150, the greater is the quantity of plaque deposited in our arteries. If the serum total cholesterol level can be prevented from rising to more than 150 mg/dl, plaques are not laid down; if elevated levels are lowered to 150 mg/dl, further plaque does not form, and parts of those present may vanish. A fruit-vegetarian-starch diet is necessary as a rule to achieve the 150 mg/dl level in most adults. Lipid-lowering drugs are required in the patients with familial hypercholesterolemia and in most patients with atherosclerotic events. The best news about atherosclerosis is that it can be prevented in those without the hereditary form, and it can be arrested by lowering elevated serum total (and LDL) cholesterol to the 150 mg/dl level.

Language of Publication

English

Unique Identifier

95390159

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MeSH Heading (Major)

Coronary Arteriosclerosis|CO/DT/ET/*PC

MeSH Heading

Acute Disease; Adult; Antilipemic Agents|EC/TU; Cholesterol|BL; Cholesterol, Dietary|AD; Female; Human; Male; Myocardial Ischemia|DT/ET; Risk Factors

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-8703

Country of Publication

UNITED STATES

Record 68 from database: MEDLINE
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Title

Role of cholesterol in regulating apolipoprotein B secretion by the liver.

Author

Thompson GR; Naoumova RP; Watts GF

Address

Clinical Sciences Centre, Royal Postgraduate Medical School, Hammersmith Hospital, London, United Kingdom.

Source

J Lipid Res, 1996 Mar, 37:3, 439-47

Abstract

The review examines the evidence that the supply of cholesterol available for incorporation into nascent lipoprotein particles exerts a regulatory influence on apolipoprotein (apo) B secretion by the liver. Support for this hypothesis comes both from in vitro experiments and from recent observations in normal subjects and patients with dyslipidemia associated with familial hypercholesterolemia, obesity, noninsulin dependent diabetes mellitus, growth hormone deficiency and cholesteryl ester storage disease. The findings do not negate a role for triglyceride synthesis in determining apoB secretion in very low density lipoprotein, but the inhibitory effects on the latter process of pharmacological blockade of cholesterol synthesis or esterification suggest that it is conditional upon an adequate supply of cholesteryl ester.

Language of Publication

English

Unique Identifier

96292463

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MeSH Heading (Major)

Apolipoproteins B|*SE; Cholesterol|BI/*PH; Liver|*SE

MeSH Heading

Acyl Coenzyme A|ME; Animal; Bile|ME; Cholesterol Esters|ME; Human; Hypercholesterolemia, Familial|ME; Lipids|ME; Lipoproteins|BI/ME; Lipoproteins, VLDL|SE; Mevalonic Acid|BL

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0022-2275

Country of Publication

UNITED STATES

Record 69 from database: MEDLINE
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Title

Regulation of hepatic apolipoprotein-B-containing lipoprotein secretion.

Author

Pease RJ; Leiper JM

Address

Department of Biochemistry and Molecular Biology, University College, London, UK.

Source

Curr Opin Lipidol, 1996 Jun, 7:3, 132-8

Abstract

The overall secretion of hepatic lipid as VLDL may be regulated by (i) changing the number of particles secreted as a result of altering apolipoprotein B output and (ii) changing the degree of lipidation of the particles with triacylglycerol so that their diameters vary over a threefold range. Substantial progress has been made in understanding the pathway of triacylglycerol incorporation into VLDL. Less is understood about the processes that commit apolipoprotein B either to secretion or to presecretory degradation, although both regulated translocation and an early lipidation step of the nascent particle with cholesterol or cholesterol ester have been implicated.

Language of Publication

English

Unique Identifier

96415599

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MeSH Heading (Major)

Apolipoproteins B|*ME; Lipoproteins|CH/*SE; Liver|*SE

MeSH Heading

Animal; Biological Transport; Carrier Proteins|ME; Cholesterol|ME; Cholesterol Esters|ME; Human; Support, Non-U.S. Gov't; Triglycerides|ME

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0957-9672

Country of Publication

UNITED STATES

Record 70 from database: MEDLINE
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Title

Pixel or death: experience from clinical trials assessing lipid lowering therapy.

Author

Barth JD

Address

Department of Medicine, University of British Columbia, Vancouver.

Source

Can J Cardiol, 1995 May, 11 Suppl C:, 9C-14C

Abstract

Repeated coronary angiography has become a surrogate for clinical events in studies involving lipid lowering treatment. Different lipid lowering interventions have resulted regression in approximately 20% of subjects. Clinical events decreased more rapidly and more profoundly than can be explained by morphological remodeling. Regression of atherosclerosis correlates well with reductions in serum low density lipoprotein (LDL) cholesterol and with increases in high density lipoprotein (HDL) cholesterol. Although overall improvement in severity and extent of the disease was modest, reduction of clinical events was impressive. Lipid modulation may stabilize existing lesions by improving the stability of the lesion cap and/or promoting loss of cholesterol content from within the plaque. Survival studies indicate that lipid lowering decreases morbidity and increases longevity in patients with established coronary artery disease. The B-mode ultrasound studies using the carotid artery as surrogate for the assessment of atherosclerosis in coronary arteries seems extremely promising. The atherosclerotic process as well as complications may be studied in an early stage using noninvasive methods.

Language of Publication

English

Unique Identifier

95269207

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MeSH Heading (Major)

Coronary Angiography|*; Coronary Arteriosclerosis|MO/*RA/TH/US; Echocardiography|*; Hyperlipidemia|*RA/TH/US

MeSH Heading

Antilipemic Agents|TU; Disease Susceptibility; Exercise Therapy; Female; Human; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Male; Risk Factors; Survival Rate; Weight Loss

Publication Type

CLINICAL TRIAL; JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0828-282X

Country of Publication

CANADA

Record 71 from database: MEDLINE
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Title

Lipoproteins and homocyst(e)ine as risk factors for atherosclerosis: assessment and treatment.

Author

Frohlich JJ

Address

St Paul's Hospital, Lipid Clinic, Vancouver, British Columbia.

Source

Can J Cardiol, 1995 May, 11 Suppl C:, 18C-23C

Abstract

Two new important independent risk factors for coronary artery disease (CAD) have been identified: lipoprotein (a) [Lp(a)] and homocyst(e)ine. Both are associated with increased frequency of cardiovascular events, both coronary and peripheral. Measurement of these two factors should be considered in patients with symptomatic CAD, stroke, a strong family history (but low other conventional risk factors); in first degree relatives of those with very high Lp(a) or homocyst(e)ine levels; and in other individuals in whom the need for an aggressive treatment of metabolic risk factors is indicated. While treatment of high serum Lp(a) with drugs is difficult it appears from the epidemiological or clinical evidence that the additional risk due to Lp(a) can be drastically lowered by decreasing the patient's low density lipoprotein (LDL) cholesterol levels to below 3 mmol/L. The treatment of increased homocyst(e)ine can be easily accomplished by vitamin B6 or folic acid administration. Various analyses describing the value of positive tests for diagnosis of atherosclerosis indicate that overall risk evaluated by computer models from Framingham data, use of total: high density lipoprotein (HDL) cholesterol ratio and/or the National Cholesterol Education Program (NCEP) II guidelines are the best predictors of future cardiovascular events. The strategic aim for treatment regimens should be threefold: lower serum LDL cholesterol levels; decrease serum triglycerides (and triglyceride-rich lipoproteins); and increase HDL cholesterol. Niacin and statin drugs are the most cost effective means to achieve the former and niacin and fibrates to achieve the latter goal. Where target LDL cholesterol levels can be achieved with less expensive statin preparations their use may be economically advantageous.

Language of Publication

English

Unique Identifier

95269200

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MeSH Heading (Major)

Antilipemic Agents|*TU; Coronary Arteriosclerosis|BL/*ET/TH; Homocysteine|*BL; Hyperlipoproteinemia|*CO/TH; Lipoprotein(a)|*BL

MeSH Heading

Female; Human; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Male; Recurrence; Risk Factors

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0828-282X

Country of Publication

CANADA

Record 72 from database: MEDLINE
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Title

Hyperlipidemia: perspectives in diagnosis and treatment.

Author

Yeshurun D; Gotto AM Jr

Address

Department of Medicine, Baylor College of Medicine, Houston, Tex. 77030, USA.

Source

South Med J, 1995 Apr, 88:4, 379-91

Abstract

Several forms of dyslipidemia are associated with premature coronary artery disease (CAD) and other vascular disease. These include elevated low-density lipoprotein cholesterol, low levels of high-density lipoprotein cholesterol, and elevated triglyceride. Because of the high incidence of CAD in many Western countries, including the United States, guidelines for managing dyslipidemia and reducing the risk of CAD have been promulgated. The National Cholesterol Education Program (NCEP) of the National Institutes of Health recently released revised guidelines for the treatment of adults with dyslipidemia, as did the European Atherosclerosis Society. Although the two reports differ in emphasis, both recommend routine screening of adults to identify specific individuals at high risk for future CAD events.

Language of Publication

English

Unique Identifier

95232574

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MeSH Heading (Major)

Hydroxymethylglutaryl CoA Reductases|*AI; Hyperlipidemia|DH/*DI/*TH

MeSH Heading

Cholestyramine|TU; Clofibrate|TU; Coronary Disease|PC; Diet, Fat-Restricted; Diet, Reducing; Exercise; Human; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Niacin|TU; Probucol|TU; Risk; Triglycerides|BL

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0038-4348

Country of Publication

UNITED STATES

Record 73 from database: MEDLINE
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Title

RSH/SLO ("Smith-Lemli-Opitz") syndrome: historical, genetic, and developmental considerations.

Author

Opitz JM

Address

Shodair Hospital, Helena, Montana.

Source

Am J Med Genet, 1994 May, 50:4, 344-6

Abstract

Thirty years after the publication of Smith et al. [1964: J Pediatr 64:210-217] of 3(4) cases of the RSH/SLO ("Smith-Lemli-Opitz") syndrome and after the publication by Roux [1964: Arch Franç Pédiatr 21:451-464] on the teratogenic action of Triparanol, a defect of cholesterol metabolism was discovered by Tint and his co-workers in the blood of the patients of Irons and Elias [Irons et al., 1993: Lancet 341:1414]. In this manner, the RSH syndrome has been identified as another metabolic multiple congenital anomalies/mental retardation (MCA/MR) syndrome (prototype Zellweger syndrome) in which deficient cholesterol synthesis must be held responsible for all parts of the syndrome, including blastogenetic and organogenetic malformations, minor anomalies, more or less severe abnormalities of CNS and PNS structure and function, postnatal failure to thrive, and, in some cases, stillbirth or infancy/childhood death.

Language of Publication

English

Unique Identifier

94270404

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MeSH Heading (Major)

Abnormalities, Multiple|*/EM/GE/ME; Lipid Metabolism, Inborn Errors|*/EM/GE; Mental Retardation|*/EM/GE/ME

MeSH Heading

Cholesterol|BI; Chromosome Mapping; Chromosomes, Human, Pair 7; Face|AB; Genitalia|AB; Human; Microcephaly; Prevalence; Syndrome

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0148-7299

Country of Publication

UNITED STATES

Record 74 from database: MEDLINE
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Title

Benefit of aggressive lipid-lowering therapy: insights from the post coronary artery bypass graft study and other trials.

Author

White CW

Address

Department of Medicine, University of Minnesota Medical School, Minneapolis 55455, USA.

Source

Am J Med, 1998 Jul 6, 105:1A, 63S-68S

Abstract

The importance of treating patients to lower cholesterol levels to lessen the risk of developing atherosclerosis is well accepted. However, the benefits of aggressive treatment for lowering low-density lipoprotein (LDL) cholesterol and a defined threshold at which lowering cholesterol is of little use are still questionable. Although definitive answers are still not available, interesting data come from follow-ups and reviews of epidemiologic and clinical trials completed decades ago. In the Seven Countries Study, a 25-year follow-up shows that while absolute levels of coronary artery disease mortality differed by geographic area, the relative increase in mortality due to a given increase in cholesterol was similar in all cultures except Japan. A new look at the Framingham Study reveals that mean serum cholesterol of persons developing coronary disease has been decreasing progressively for the last 3 decades. Most recently, average levels of total serum cholesterol and LDL cholesterol for men are below the levels now recommended for treatment according to the National Cholesterol Education Program guidelines. Clinical and angiographic intervention trials have now ascertained that lowering LDL cholesterol is effective in prevention and in secondary treatment of coronary atherosclerosis. Recent reviews of the Scandinavian Simvastatin Survival Study (4S), the Cholesterol and Recurrent Events (CARE) study, Holme's meta-analysis of 42 randomized cholesterol-lowering trials, Roussouw's meta-analysis of 14 angiographic trials, and the Harvard Atherosclerosis Reversibility Project retrospectively validate the effectiveness of treatment and point to those patient populations in which treatment is most effective. The Post Coronary Artery Bypass Graft (Post CABG) trial evaluated aggressive LDL cholesterol-lowering therapy versus moderate treatment goals, and definitively demonstrated that in patients with a moderate increase in serum cholesterol, aggressive lipid lowering compares very positively with a moderate strategy. The benefits of decreasing cholesterol to very low levels are not yet certain, although epidemiologic reviews strongly correlate lower cholesterol levels with lowered coronary artery disease mortality. Meta-analyses confirm that LDL cholesterol lowering is at least as effective in low-risk patients as in those at high risk. Review of the Post CABG trial comes closest to providing practitioners with clinical guidelines.

Language of Publication

English

Unique Identifier

98370767

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MeSH Heading (Major)

Anticholesteremic Agents|*TU; Coronary Artery Bypass|*; Coronary Disease|BL/*PC/RA/SU; Lipoproteins, LDL Cholesterol|*BL/*DE

MeSH Heading

Age Factors; Clinical Trials; Coronary Angiography; Human; Sex Factors

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9343

Country of Publication

UNITED STATES

CAS Registry/EC Number

0 (Anticholesteremic Agents); 0 (Lipoproteins, LDL Cholesterol)

Record 75 from database: MEDLINE
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Title

Effect of pyruvate and dihydroxyacetone on metabolism and aerobic endurance capacity.

Author

Ivy JL

Address

Department of Kinesiology and Health Education, University of Texas at Austin, USA. JohnIvy@mail.utexas.edu

Source

Med Sci Sports Exerc, 1998 Jun, 30:6, 837-43

Abstract

Pyruvate and dihydroxyacetone are three carbon compounds that when infused directly into the blood or taken orally produce strong metabolic effects. When chronically fed to animals as part of their diet, pyruvate plus dihydroxyacetone reduce the rate of weight gain and body fat content during growth. These alterations in growth pattern appear to be the result of an increased loss of calories as heat at the expense of storage of lipid. Pyruvate-dihydroxyacetone supplementation has also been found to improve the insulin sensitivity of insulin resistant rats and reduce plasma cholesterol levels induced by a high cholesterol diet as well as lower blood pressure and heart rate in obese individuals. When infused in rats during prolonged treadmill running, pyruvate reduced run time to exhaustion by approximately 67%. However, when provided as an oral supplement for several days, it has enhanced aerobic endurance capacity. The mechanism of action is unclear, but available data suggest that the increase in performance following pyruvate-dihydroxyacetone supplementation may be a result of an increased reliance on blood glucose, thus sparing muscle glycogen. In summary, chronic supplementation of pyruvate-dihydroxyacetone may be beneficial from a preventive medicine prospective as well as for certain athletic endeavors.

Language of Publication

English

Unique Identifier

98287736

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MeSH Heading (Major)

Dihydroxyacetone|*PD; Exercise|*PH; Physical Conditioning, Animal|*PH; Physical Endurance|*DE/PH; Pyruvic Acid|*PD

MeSH Heading

Animal; Cholesterol|BL/ME; Glycogen|ME; Human; Insulin Resistance|PH; Muscle, Skeletal|ME; Preventive Medicine; Rats

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0195-9131

Country of Publication

UNITED STATES

Record 76 from database: MEDLINE
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Title

Diet and cardiovascular disease prevention: what works?

Author

Van Horn L; Kavey RE

Address

Department of Preventive Medicine, Northwestern University Medical School, Chicago, IL 60611-4402, USA.

Source

Ann Behav Med, 1997 Sum, 19:3, 197-212

Abstract

Diet is routinely recommended as the primary strategy for the prevention and treatment of high blood cholesterol. The National Cholesterol Education Program (NCEP), the American Heart Association (AHA), and a host of other health and medical organizations have advocated a diet low in total and saturated fat and cholesterol for reducing risk of cardiovascular disease. What is the evidence supporting these guidelines and the expected efficacy of dietary treatment? There is growing awareness that despite well-documented rationale for the dietary approach, many eligible patients are not routinely prescribed dietary treatment, and among those who are, there is limited response. What are the obstacles in implementing effective dietary intervention for prevention of cardiovascular disease? What are both the theoretical and practical limitations to achieving long-term adherence to diet and what strategies have been shown to be most effective? A review of the data surrounding these diet-lipid relationships is presented along with recently tested and promising behavioral approaches to facilitating patient adherence.

Language of Publication

English

Unique Identifier

98262356

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MeSH Heading (Major)

Cardiovascular Diseases|DH/*PC/PX; Food Habits|*/PX

MeSH Heading

Cholesterol, Dietary|AD/AE; Diet, Fat-Restricted; Human; Hypercholesterolemia|DH/PC/PX; Patient Compliance|PX; Risk Factors; Treatment Outcome

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0883-6612

Country of Publication

UNITED STATES

Record 77 from database: MEDLINE
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Title

Suicide: a four-pathway clinical-biochemical model.

Author

Fawcett J; Busch KA; Jacobs D; Kravitz HM; Fogg L

Address

Department of Psychiatry, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois 60612, USA. jfawcett@rush.edu

Source

Ann N Y Acad Sci, 1997 Dec, 836:, 288-301

Abstract

This chapter, based on a review of recent research as well as data presented in this report, proposes four hypothetical pathways leading to suicide in clinical depression: (1) an acute pathway involving severe anxiety/agitation associated with high brain corticotrophin-releasing factor (CRF or CRH) levels, (2) trait baseline and reactivity hopelessness, (3) severe anhedonia, and (4) trait impulsiveness associated with low brain serotonin turnover and low total cholesterol as a possible peripheral correlate. Clinical research showing evidence for acute versus chronic high-risk suicide factors and other studies linking severe anxiety/agitation to high CRF levels will be presented as associated with acute suicidal risk, which is potentially reversible with recognition and treatment. Evidence for anhedonia severity as a risk factor and trait, as well as evidence that baseline hopelessness and sensitivity are traits related to chronic suicide risk, will be presented. Finally, evidence relating low serum cholesterol to suicide in depressed inpatients will be presented in the context of literature suggesting a relationship between low serum cholesterol and violent death and suicide in population studies. Data suggesting a relationship between low serum cholesterol and decreased CSF 5-HIAA, suggesting reduced serotonin turnover, will be presented, in light of prior studies relating low CSF 5-HIAA and violent suicide. These data taken together suggest four pathways to suicide that are worth investigating in order to better understand the mechanisms leading to this behavior. Future possibilities and applications of these findings are discussed.

Language of Publication

English

Unique Identifier

98279777

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MeSH Heading (Major)

Models, Neurological|*; Suicide|*

MeSH Heading

Cholesterol|BL/PH; Depressive Disorder|PP; Human; Hypothalamo-Hypophyseal System|PP; Pituitary-Adrenal System|PP; Risk Factors; Serotonin|PH

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0077-8923

Country of Publication

UNITED STATES

Record 78 from database: MEDLINE
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Title

Cholesterol and coronary heart disease in women.

Author

Lewis SJ

Address

Portland Cardiovascular Institute, Oregon, USA.

Source

Cardiol Clin, 1998 Feb, 16:1, 9-15

Abstract

Coronary heart disease (CHD) is the leading cause of death for women. Early studies suggested that CHD was more benign in women than in men. These early studies resulted in limited availability of studies of coronary risk prevention and lipid lowering on women. The realization that women are at high risk for CHD events, however, has led to increased data on the benefit of risk prevention and cholesterol lowering in women. Current data support recommendations for aggressive lipid lowering in women with existing CHD, or who are at risk for developing CHD.

Language of Publication

English

Unique Identifier

98168620

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MeSH Heading (Major)

Cholesterol|*BL; Coronary Disease|BL/*EP

MeSH Heading

Aged; Cholesterol, Dietary|AD; Female; Human; Male; Middle Age; Risk Factors; Sex Factors

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0733-8651

Country of Publication

UNITED STATES

Record 79 from database: MEDLINE
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Title

Decreased cholesterol efflux from fibroblasts of a patient without Tangier disease, but with markedly reduced high density lipoprotein cholesterol levels.

Author

Eberhart GP; Mendez AJ; Freeman MW

Address

Lipid Metabolism Unit, Massachusetts General Hospital, Boston 02114, USA.

Source

J Clin Endocrinol Metab, 1998 Mar, 83:3, 836-46

Abstract

A 51-yr-old woman without clinical evidence of Tangier disease, but with an extremely low high density lipoprotein (HDL) cholesterol level, was studied. No defect in the major structural protein of HDL, apolipoprotein AI (apo AI), was detected. A preponderance of small HDL particles in the patient's plasma suggested defective uptake of cellular cholesterol. Efflux of [3H]cholesterol from patient fibroblasts to normal apo AI was decreased 50%. Cholesterol efflux to HDL was also decreased, but efflux to trypsin-modified HDL was not. The patient's cells partitioned more exogenously provided [3H]cholesterol into free cholesterol and synthesized greater amounts of phosphatidylcholine than did normal or Tangier fibroblasts. Her fibroblasts did not differ from normal fibroblasts in sterol synthesis rate, cellular cholesterol and cholesterol ester content, or incorporation of oleate into cholesterol ester. The data indicate the presence of a defect in apolipoprotein-dependent cellular cholesterol efflux that differs from that seen in Tangier disease. These findings are the first evidence that other low HDL cholesterol syndromes, besides Tangier disease, may also be associated with cholesterol efflux abnormalities. The identification of mutant genes responsible for apolipoprotein-mediated efflux abnormalities should provide valuable insights into cellular mechanisms involved in the reverse cholesterol transport pathway.

Language of Publication

English

Unique Identifier

98165581

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MeSH Heading (Major)

Cholesterol|*ME; Fibroblasts|*ME; Lipoproteins, HDL Cholesterol|*BL/CH

MeSH Heading

Apolipoprotein A-I|BL; Case Report; DNA|AN; Female; Human; Middle Age; Particle Size; Support, U.S. Gov't, P.H.S.; Tangier Disease|ME

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0021-972X

Country of Publication

UNITED STATES

Record 80 from database: MEDLINE
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Title

Serum low-density lipoprotein cholesterol response to modification of saturated fat intake: recent insights.

Author

Cater NB; Garg A

Address

Center for Human Nutrition, University of Texas Southwestern Medical Center at Dallas 75235-9052, USA.

Source

Curr Opin Lipidol, 1997 Dec, 8:6, 332-6

Abstract

Two lines of investigation have provided important insights into dietary therapy of hypercholesterolemia. Studies have confirmed the efficacy of the US National Cholesterol Education Program Step II diet in lowering serum LDL-cholesterol concentrations and demonstrate that wide variability exists in responsiveness to this diet. Other studies indicate that, contrary to expectations, cholesterol raising saturated fatty acids are not limited to long-chain saturates, but also include medium-chain and very long-chain saturated fatty acids.

Language of Publication

English

Unique Identifier

98074252

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MeSH Heading (Major)

Dietary Fats|*AD; Hypercholesterolemia|BL/*DH; Lipoproteins, LDL Cholesterol|*BL

MeSH Heading

Adult; Cholesterol, Dietary|AD; Fatty Acids|AD/CH; Female; Human; Male; Middle Age; Patient Education; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0957-9672

Country of Publication

UNITED STATES

Record 81 from database: MEDLINE
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Title

Effects of cocoa butter on serum lipids in humans: historical highlights.

Author

Denke MA

Address

Center for Human Nutrition, University of Texas Southwestern Medical Center at Dallas 75235-9052.

Source

Am J Clin Nutr, 1994 Dec, 60:6 Suppl, 1014S-1016S

Abstract

It has been known for some time that cocoa butter, although rich in saturated fatty acids, does not raise total serum cholesterol concentrations as much as expected from its total saturated fatty acid content. Whether the effect of cocoa butter feeding on low-density-lipoprotein- (LDL)-cholesterol concentrations was also less than predicted by its total saturated fatty acid content needed to be tested. In a recent experiment cocoa butter did not raise LDL cholesterol as much as predicted by its total saturated fatty acid content. However, because of its significant palmitic acid content, cocoa butter did raise LDL-cholesterol concentrations more than do most liquid vegetable oils.

Language of Publication

English

Unique Identifier

95067736

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MeSH Heading (Major)

Cholesterol|*BL; Dietary Fats|AD/*ME

MeSH Heading

Human; Lipoproteins, LDL Cholesterol|BL; Stearic Acids|AD/ME

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9165

Country of Publication

UNITED STATES

Record 82 from database: MEDLINE
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Title

Position paper on trans fatty acids. ASCN/AIN Task Force on Trans Fatty Acids. American Society for Clinical Nutrition and American Institute of Nutrition.

Address

Source

Am J Clin Nutr, 1996 May, 63:5, 663-70

Abstract

This report addresses the current controversy about possible health hazards of dietary trans fatty acid isomers, which are created during hydrogenation of unsaturated fats to change their textural properties and melting points. Estimates of intakes are approximations based on limited data and problematic analytic techniques. Major contributors in the diet are fried and baked foods and margarine, in which partially hydrogenated vegetable oils may replace fat sources richer in saturated fatty acids and cholesterol. Consumption of trans fatty acids in the United States has been relatively constant, and new food technologies are yielding decreases in the trans fatty acid content of commercially prepared foods. When intake of trans fatty acids (as hydrogenated fat) is compared with that of saturated fat, total and low-density-lipoprotein (LDL)-cholesterol concentrations in blood are lower, but both trans fats and saturated fats increase total and LDL concentrations when compared with cis fatty acids or native unhydrogenated fat. Epidemiologic data are conflicting with respect to cardiovascular disease outcomes. We cannot conclude that the intake of trans fatty acids is a risk factor for coronary heart disease nor can we expect that substituting trans- for cis-containing fats will reduce the risk of coronary heart disease. Few rigorous studies have dealt with biomedical effects of trans fatty acids and possible mechanisms relevant to human health and diseases. The nutrition labeling issue is unresolved. The options, recommendations, and research suggestions in this report should outline for nutrition scientists the database needed before any new dietary recommendations or changes in nutrition policy concerning trans fatty acids can be made. The debate about trans fatty acids should not detract from dietary recommendations to limit the intake of saturated fat and total fat.

Language of Publication

English

Unique Identifier

96204942

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MeSH Heading (Major)

Dietary Fats|AD/*ST; Fatty Acids|AD/*CH; Nutrition Policy|*

MeSH Heading

Cardiovascular Diseases|BL/EP/ET; Fatty Acids, Unsaturated|BL/ME; Human; Hydrogenation; Incidence; Isomerism; Lipoproteins, LDL Cholesterol|BL/ME; Risk Factors; United States|EP

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9165

Country of Publication

UNITED STATES

Record 83 from database: MEDLINE
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Title

Hydroxypropylmethylcellulose, viscosity, and plasma cholesterol control.

Author

Topping D

Address

CSIRO Australia, Division of Human Nutrition, Glenthorne Laboratory.

Source

Nutr Rev, 1994 May, 52:5, 176-8

Abstract

The mechanism for the lowering of plasma cholesterol by water-soluble nonstarch polysaccharides (NSP) could involve alteration of intestinal viscosity leading to attenuated fat and steroid digestion and absorption. Alternatively, there may be direct inhibition of hepatic cholesterol synthesis by short-chain fatty acids produced by large bowel bacterial fermentation. A synthetic NSP, hydroxypropylmethylcellulose (HPMC), has been shown to lower plasma low-density lipoprotein (LDL) cholesterol in humans. This polysaccharide is not fermented by the large bowel microflora and has been shown to lower the plasma and liver cholesterol in hamsters, with no change noted in hepatic sterol synthesis. In further studies with hamsters, a linear relationship has been identified between plasma cholesterol and the logarithm of hydroxymethylcellulose viscosity. Only a relatively small increment in viscosity was necessary to achieve a maximal effect, suggesting that intestinal digestion may be quite sensitive to increased NSP intake.

Language of Publication

English

Unique Identifier

94329353

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MeSH Heading (Major)

Gastrointestinal Contents|*CH; Hypercholesterolemia|*DT; Lactose|*AA/CH/TU; Lipoproteins, LDL Cholesterol|*BL; Methylcellulose|*AA/CH/TU

MeSH Heading

Animal; Cholesterol|BL; Female; Human; Male; Solubility; Viscosity

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0029-6643

Country of Publication

UNITED STATES

Record 84 from database: MEDLINE
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Title

Cross-sectional and longitudinal changes in total and high-density-lipoprotein cholesterol levels over a 20-year period in elderly men: the Honolulu Heart Program.

Author

Abbott RD; Sharp DS; Burchfiel CM; Curb JD; Rodriguez BL; Hakim AA; Yano K

Address

Division of Biostatistics, University of Virginia School of Medicine, Charlottesville 22908, USA.

Source

Ann Epidemiol, 1997 Aug, 7:6, 417-24

Abstract

PURPOSE: The purpose of this report is to describe levels of total cholesterol and high-density-lipoprotein cholesterol (HDL-C) in a group of elderly men and to compare these levels to those that were observed 20 years earlier. METHODS: From 1965-1968, the Honolulu Heart Program began following 8006 men of Japanese ancestry living on the island of Oahu, Hawaii, in a prospective study of coronary heart disease and stroke. This report presents data for 971 men who participated in a separate fasting study of lipids and lipoproteins that first occurred from 1970-1972 and in those who received repeat examinations 10 and 20 years later. Men were aged 71-93 years at the last examination. RESULTS: Over the 20-year period, total cholesterol declined by 1.6-1.8 mg/dL per year (P < 0.001), from average baseline values of 219-222 mg/dL. Levels of HDL-C rose 0.2-0.3 mg/dL per year (P < 0.001), from average baseline values of 44-46 mg/dL. After adjustment for baseline cholesterol levels, men with prevalent coronary heart disease at the end of the 20-year follow-up experienced significantly greater reductions in total cholesterol levels than men without disease (P < 0.001). Men who developed coronary heart disease within the first 10 years of follow-up had the greatest yearly decline in total cholesterol (1.9 mg/dL), followed by men who developed heart disease later (1.8 mg/dL) and men who remained disease free (1.5 mg/dL). Differences between men with recent and earlier disease were not statistically significant, although men without coronary disease experienced a significantly smaller decrease in total cholesterol than either of these groups (P < 0.05). CONCLUSIONS: Changes in total cholesterol and HDL-C levels with advancing age may be part of a natural aging process. Some changes, however, such as large reductions in total cholesterol, may signal occult disease or declines in overall health. Selective survival may contribute to these findings since improvements in lipid and lipoprotein levels that are beneficial in younger ages were common in this long-lived cohort of men.

Language of Publication

English

Unique Identifier

97425401

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MeSH Heading (Major)

Aging|*BL; Cholesterol|*BL; Coronary Disease|*BL/EP

MeSH Heading

Aged; Aged, 80 and over; Comparative Study; Cross-Sectional Studies; Hawaii|EP; Human; Japan|EH; Linear Models; Lipoproteins, HDL Cholesterol|BL; Longitudinal Studies; Male; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

1047-2797

Country of Publication

UNITED STATES

Record 85 from database: MEDLINE
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Title

Diet and coronary heart disease: beyond dietary fats and low-density-lipoprotein cholesterol.

Author

Fraser GE

Address

Center for Health Research, Loma Linda University, School of Public Health, CA.

Source

Am J Clin Nutr, 1994 May, 59:5 Suppl, 1117S-1123S

Abstract

Traditionally, the effects of diet on coronary heart disease have been attributed to the effects of medium-chain fatty acids, soluble fiber, and dietary cholesterol on serum low-density-lipoprotein (LDL) cholesterol concentrations. We review evidence here that many other dietary substances may affect risk, often via mechanisms not involving LDL-cholesterol concentrations directly. Such substances include phytosterols, tocotrienols, arginine, and antioxidant vitamins. The effects of diet on high-density-lipoprotein-cholesterol concentrations, triglycerides (fasting and postprandial), oxidized LDL particles, prostaglandins, and endothelium-derived relaxing factor are described. Finally, an illustration of some epidemiologic associations between diet and coronary disease events is made from the Adventist Health Study data.

Language of Publication

English

Unique Identifier

94226073

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MeSH Heading (Major)

Coronary Disease|*/ET/PC; Diet|*; Dietary Fats|*AD/PD; Lipoproteins, LDL Cholesterol|*BL

MeSH Heading

Adult; Aged; Aged, 80 and over; Cholesterol|BL; Christianity; Endothelium-Derived Relaxing Factor|PH; Female; Human; Male; Middle Age; Support, U.S. Gov't, P.H.S.; Vegetarianism

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9165

Country of Publication

UNITED STATES

Record 86 from database: MEDLINE
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Title

Regulation of cholesterol biosynthesis by diet in humans.

Author

Jones PJ

Address

School of Dietetics and Human Nutrition, Faculty of Agricultural and Environmental Sciences, McGill University, Ste-Anne-de-Bellevue, Quebec, Canada. jonesp@agradm.lan.mcgill.ca

Source

Am J Clin Nutr, 1997 Aug, 66:2, 438-46

Abstract

Biosynthesis of cholesterol represents a major input into whole-body pools; however, its regulation has been difficult to study in humans because of limitations in methodologies. The present objectives are to compare available techniques for measuring this process and examine how dietary factors alter human cholesterol biosynthesis. Review of existing techniques suggests that mass isotopomer distribution analysis and deuterium incorporation approaches offer advantages over other methods. Dietary factors influencing human cholesterol synthesis include energy restriction, meal frequency, dietary fat type, and cholesterol and phytosterol content. Food deprivation for as short as 24 h results in almost complete cessation of cholesterol biosynthesis. Similarly, increased meal frequency patterns are associated with a substantial depression in synthesis. In contrast, consumption of oils rich in polyunsaturated fatty acids, despite reducing circulating concentrations, increases the cholesterol synthesis rate compared with other fats. Stepwise addition of dietary cholesterol is associated with only a modest decline in cholesterogenesis while raising plasma concentrations slightly. It can be concluded that synthesis, as a contributor to circulating cholesterol concentrations, is sensitive to many dietary factors. Energy deprivation results in the greatest decline in synthesis, likely accounting for the beneficial decline in circulating cholesterol concentrations observed with weight loss.

Language of Publication

English

Unique Identifier

97393691

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MeSH Heading (Major)

Cholesterol|*BI; Diet|*

MeSH Heading

Cholesterol, Dietary|AD; Dietary Fats|AD; Energy Intake; Fatty Acids|AD; Human; Plants|CH

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9165

Country of Publication

UNITED STATES

Record 87 from database: MEDLINE
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Title

The effect of dietary fat, antioxidants, and pro-oxidants on blood lipids, lipoproteins, and atherosclerosis.

Author

Kwiterovich PO Jr

Address

Johns Hopkins University School of Medicine, Department of Pediatrics and Medicine, Baltimore, MD 21287-3654, USA.

Source

J Am Diet Assoc, 1997 Jul, 97:7 Suppl, S31-41

Abstract

A number of primary and secondary prevention trials, including angiographic studies, have indicated that a decrease in dietary saturated fat and cholesterol produces a decrease in the blood levels of cholesterol and low-density lipoprotein (LDL) cholesterol, leading to a decrease in coronary artery disease (CAD). Increasing evidence indicates that the oxidation of LDL in human beings is atherogenic. Of the three major antioxidants, vitamin E, beta carotene, and vitamin C, the evidence is strongest that vitamin E (at a minimum dose of 100 IU/day) has a strong and independent inverse association with CAD. Selenium and flavonoids also have antioxidant properties, but their association with CAD in human beings is equivocal. Two prooxidants, homocysteine and iron, have been found to be associated with CAD. Blood homocysteine levels can be lowered significantly by an increase in dietary folic acid. Clinical trials are needed to assess expeditiously the effect of antioxidants, particularly vitamin E, and of folic acid on CAD and atherosclerosis. The substitution of monounsaturated fat for saturated fat lowers LDL and makes it less susceptible to oxidation without decreasing high-density lipoprotein (HDL) cholesterol. Studies in transgenic mice indicate that apolipoprotein A-I, the major protein of HDL, may inhibit the oxidation of LDL. Dietary trans fatty acids at the level consumed by many Americans can increase LDL cholesterol and may decrease HDL cholesterol. Individuals who have CAD or have family members who have premature CAD have delayed clearance of dietary fat, as judged by studies of postprandial triglyceride metabolism. The importance of decreasing dietary saturated fat and cholesterol is well established, but a number of other factors appear to influence the risk of CAD significantly and provide important areas for future investigation to improve prevention and treatment through better nutrition.

Language of Publication

English

Unique Identifier

97359649

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MeSH Heading (Major)

Antioxidants|*AD/PD; Atherosclerosis|BL/*PC; Dietary Fats|*AD/PD; Lipids|*BL; Lipoproteins|*BL; Oxidants|*AD/PD

MeSH Heading

Animal; Cholesterol, Dietary|AD/AE; Clinical Trials; Human; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-8223

Country of Publication

UNITED STATES

Record 88 from database: MEDLINE
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Title

Dietary phytosterols: a review of metabolism, benefits and side effects.

Author

Ling WH; Jones PJ

Address

School of Dietetics and Human Nutrition, McGill University at Macdonald Campus, Ste-Anee-de-Bellevue, PQ, Canada.

Source

Life Sci, 1995, 57:3, 195-206

Abstract

Most animal and human studies show that phytosterols reduce serum/or plasma total cholesterol and low density lipoprotein (LDL) cholesterol levels. Phytosterols are structurally very similar to cholesterol except that they always contain some substitutions at the C24 position on the sterol side chain. Plasma phytosterol levels in mammalian tissue are normally very low due primarily to poor absorption from the intestine and faster excretion from liver compared to cholesterol. Phytosterols are able to be metabolized in the liver into C21 bile acids via liver other than normal C24 bile acids in mammals. It is generally assumed that cholesterol reduction results directly from inhibition of cholesterol absorption through displacement of cholesterol from micelles. Structure-specific effects of individual phytosterol constituents have recently been shown where saturated phytosterols are more efficient compared to unsaturated compounds in reducing cholesterol levels. In addition, phytosterols produce a wide spectrum of therapeutic effects in animals including anti-tumour properties. Phytosterols have been shown experimentally to inhibit colon cancer development. With regard to toxicity, no obvious side effects of phytosterol have been observed in studies to date, except in individual with phytosterolemia, an inherited lipid disorder. Further characterization of the influence of various phytosterol subcomponents on lipoprotein profiles in humans is required to maximize the usefulness of this non-pharmacological approach to reduction of atherosclerosis in the population.

Language of Publication

English

Unique Identifier

95319262

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MeSH Heading (Major)

Diet|*; Phytosterols|AE/ME/*PD

MeSH Heading

Animal; Antineoplastic Agents|PD; Cholesterol|BL/ME; Human; Intestinal Absorption; Lipoproteins|BI/BL; Sterol O-Acyltransferase|ME

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0024-3205

Country of Publication

ENGLAND

Record 89 from database: MEDLINE
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Title

Response of low density lipoprotein cholesterol levels to dietary change: contributions of different mechanisms.

Author

Fielding CJ

Address

Cardiovascular Research Institute, University of California, San Francisco 94143, USA.

Source

Curr Opin Lipidol, 1997 Feb, 8:1, 39-42

Abstract

In many individuals, LDL-cholesterol levels rise following increased consumption of dietary cholesterol or saturated and trans-monounsaturated fatty acids. In others, a reduction of cholesterogenesis fully compensates for these effects. In responding individuals, much of the increase in LDL-cholesterol observed may result directly from an increase in plasma cholesteryl ester transfer protein activity whose effect is not mediated by hepatic LDL receptors.

Language of Publication

English

Unique Identifier

97273230

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MeSH Heading (Major)

Cholesterol, Dietary|*AD; Dietary Fats|*AD; Lipoproteins, LDL Cholesterol|BI/*BL

MeSH Heading

Carrier Proteins|BL; Down-Regulation (Physiology); Fatty Acids|AD; Human

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0957-9672

Country of Publication

UNITED STATES

Record 90 from database: MEDLINE
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Title

Abnormal cholesterol metabolism in Smith-Lemli-Opitz syndrome.

Author

Elias ER; Irons M

Address

Boston Floating Hospital for Children at Tufts-New England Medical Center, Massachusetts 02111, USA.

Source

Curr Opin Pediatr, 1995 Dec, 7:6, 710-4

Abstract

Smith-Lemli-Opitz syndrome (SLOS) is a common autosomal recessive disorder. Children with SLOS present with specific facial dysmorphism and have multiple congenital anomalies including cleft palate, congenital heart disease, genitourinary anomalies, and limb abnormalities. They also manifest severe failure to thrive and mental retardation. A metabolic defect at the final step in the cholesterol biosynthetic pathway has been described in SLOS patients. This defect results in markedly reduced cholesterol levels and abnormal accumulation of cholesterol precursors, particularly 7-dehydrocholesterol. This newly described metabolic defect in humans is one of only a few metabolic errors known to cause multiple birth defects. The biochemical profile of reduced plasma cholesterol levels in association with markedly elevated levels of the cholesterol precursor 7-dehydrocholesterol is now used to confirm the diagnosis of SLOS, which was formerly made on purely clinical grounds. This biochemical abnormality has been confirmed in dozens of patients with SLOS in both the United States and Europe. The severe cholesterol deficiency seen in these patients has multiple effects on health and early childhood development, because cholesterol is an essential component of many cell functions, which explains many of the clinical findings seen in SLOS.

Language of Publication

English

Unique Identifier

96372201

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MeSH Heading (Major)

Cholesterol|BI/BL/*DF; Metabolism, Inborn Errors|*ME; Smith-Lemli-Opitz Syndrome|*ME/TH

MeSH Heading

Animal; Child; Human

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

1040-8703

Country of Publication

UNITED STATES

Record 91 from database: MEDLINE
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Title

Cytochrome P450 in the brain: neuroendocrine functions.

Author

Warner M; Gustafsson JA

Address

Department of Medical Nutrition, Karolinska Institute Novum, Huddinge, Sweden.

Source

Front Neuroendocrinol, 1995 Jul, 16:3, 224-36

Abstract

The effectiveness of steroid hormone metabolites as sedatives and anesthetics has been known for many years. More recently, their interaction with neurotransmitter receptors has helped to elucidate their mechanism of action, but their physiological functions and their role in disturbances of behavior, anxiety, and sleep/wakefulness have yet to be elucidated. Until 1981 it was assumed that metabolites of steroid hormones arose from the adrenals and gonads and that their action on neurotransmitter receptors was a mechanism of communication between the brain and the periphery. The evidence that the brain could accumulate steroids independently of the adrenals and gonads in 1981 and later the evidence for the presence of the cholesterol side chain cleavage enzyme (P450scc) in the brain have challenged this concept and stimulated a great deal of interest in the possibility that the brain could be making its own steroids from cholesterol for some as yet undefined purpose. In this review we examine the data pertaining to the role of brain P450 in the synthesis and degradation of neurosteroids. We summarize the data on the presence of P450scc in the brain and try to answer the following questions: (1) Does P450scc in the brain contribute significantly to the synthesis of GABAA receptor active steroids? (2) Can the P450scc in the brain account for the accumulation of pregnenolone in the brain? (3) Is there evidence for special functions of the pregnenolone synthesized in the brain? (4) Is there a role for other forms of brain P450 in neurosteroid action?

Language of Publication

English

Unique Identifier

96047662

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MeSH Heading (Major)

Brain|*EN; Cytochrome P-450|*ME; Neurosecretory Systems|*PH

MeSH Heading

Animal; Cholesterol Monooxygenase (Side-Chain-Cleaving)|AN/ME; Human; Prasterone|BI; Pregnenolone|BI; Steroid 17 alpha-Monooxygenase|AN/ME; Steroids|ME; Support, Non-U.S. Gov't

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0091-3022

Country of Publication

UNITED STATES

Record 92 from database: MEDLINE
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Title

Cholesterol emboli: a common cause of renal failure.

Author

Vidt DG

Address

Department of Nephrology/Hypertension, Cleveland Clinic Foundation, Ohio 44195, USA.

Source

Annu Rev Med, 1997, 48:, 375-85

Abstract

Cholesterol embolization (CE), usually occurring in males in their sixth or seventh decade of life, can affect multiple organ systems, including the kidney. Interventive diagnostic procedures and aortic surgery greatly increase the risk of CE. Rapid or insidious progression of renal failure in association with surgical or diagnostic radiologic procedures should suggest this diagnosis. Progressive renal insufficiency in older patients with generalized arterial disease should suggest ischemic nephropathy secondary to bilateral renal artery stenosis, renal CE, or both. Recent worsening of hypertension is characteristic of either diagnosis. A number of clinical conditions can simulate renal CE, and final differentiation may be possible only by renal biopsy. Aggressive, supportive management of renal CE is warranted because renal function may stabilize and, in a limited number of cases, may even improve.

Language of Publication

English

Unique Identifier

97198994

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MeSH Heading (Major)

Embolism, Cholesterol|*CO/DI/TH; Kidney Failure, Chronic|DI/*ET/TH

MeSH Heading

Aged; Biopsy; Diagnosis, Differential; Human; Kidney Glomerulus|PA; Risk Factors

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0066-4219

Country of Publication

UNITED STATES

Record 93 from database: MEDLINE
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Title

Effects of dietary fatty acids on lipoproteins and cardiovascular disease risk: summary.

Author

Schaefer EJ

Address

Lipid Metabolism Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, Boston, MA 02111, USA.

Source

Am J Clin Nutr, 1997 May, 65:5 Suppl, 1655S-1656S

Abstract

Cardiovascular disease is the leading cause of death and disability in the United States and other countries. To reduce the risk of cardiovascular disease, dietary saturated fat and cholesterol should be reduced. This section of the workshop included a discussion of pragmatic issues associated with translating complex scientific information on the fat and fatty acid content of foods for the public; an overview of and a theoretical framework for cholesterol and lipoprotein metabolism; information on the role of cholesterol in the control of low-density-lipoprotein cholesterol (from animal studies); epidemiologic studies on the association between dietary fat and fatty acids and lipids and lipoproteins; the appropriate experimental design for fatty acid studies; and clinical studies evaluating the effects of individual fatty acids on plasma lipids and lipoproteins. The evidence to date indicates that the individual fatty acids elicit distinctly different physiologic effects. There is still much to be learned about the effects of individual fatty acids on lipids and lipoproteins, their metabolic fate, and the responsible biological mechanisms.

Language of Publication

English

Unique Identifier

97275735

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MeSH Heading (Major)

Cardiovascular Diseases|*BL/*EP; Dietary Fats|*PD; Fatty Acids|*PD; Lipoproteins|*BL/ME

MeSH Heading

Animal; Cholesterol|BL/ME; Human; Risk Factors; United States|EP

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9165

Country of Publication

UNITED STATES

Record 94 from database: MEDLINE
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Title

Effects of dietary fat and fatty acids on coronary artery disease risk and total and lipoprotein cholesterol concentrations: epidemiologic studies.

Author

Caggiula AW; Mustad VA

Address

Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, PA 15261, USA.

Source

Am J Clin Nutr, 1997 May, 65:5 Suppl, 1597S-1610S

Abstract

Because of their large sample sizes, epidemiologic studies can provide important data on the relation between diet, specifically dietary fat and fatty acids, and lipid and lipoprotein concentrations as well as the incidence of coronary artery disease. Although correlation coefficients vary widely (from 0.84 to 0.01) and are frequently low between dietary variables and coronary artery disease or lipids and lipoprotein fractions in the studies reviewed here, intakes of saturated fatty acids and dietary cholesterol are generally positively correlated with blood cholesterol in men and women. Associations between other fatty acids are less consistent and may be related to the considerable differences in these studies in dietary methodologies used, databases used for analyses, and homogeneity of intakes within populations. Relatively few data are available for women, cultural minorities within the United States, or young or elderly populations. However, the trends observed in the United States, ie, lower rates of coronary artery disease as well as lower reported intakes of both total and saturated fats, support the relations observed in the epidemiologic studies.

Language of Publication

English

Unique Identifier

97275730

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MeSH Heading (Major)

Cholesterol|*BL; Coronary Disease|BL/*EP/ET; Dietary Fats|*PD; Fatty Acids|*PD

MeSH Heading

Adolescence; Adult; Aged; Aged, 80 and over; Case-Control Studies; Child; Cholesterol, Dietary|PD; Cohort Studies; Female; Human; Incidence; Male; Middle Age; Population; Prospective Studies; Risk Factors; United States|EP

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9165

Country of Publication

UNITED STATES

Record 95 from database: MEDLINE
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Title

Prevention of coronary heart disease through cholesterol reduction.

Author

Grundy SM

Address

University of Texas Southwestern Medical Center, Dallas, USA.

Source

Am Fam Physician, 1997 May, 55:6, 2250-8

Abstract

Growing evidence suggests that lowering serum cholesterol levels, particularly low-density lipoprotein levels, will reduce the risk for coronary heart disease. The benefit of cholesterol-lowering therapy has been documented by many clinical trials. Two secondary prevention trials, the Scandinavian Simvastatin Survival Study and the Cholesterol and Recurrent Events trial, demonstrated a striking reduction in recurrent coronary heart disease without an increase in noncardiovascular mortality; treatment with simvastatin reduced total mortality by 30 percent. A primary prevention trial, the West of Scotland Coronary Prevention Study, demonstrated similar results in high-risk patients without established coronary heart disease. More recent angiographic trials revealed that cholesterol-lowering therapy will reduce progression of atherosclerosis and, in some cases, will reverse existing lesions. Use of HMG-CoA reductase inhibitors also appears to be beneficial and safe. Evidence supports cholesterol-lowering therapy in high-risk patients, both with and without established atherosclerotic disease.

Language of Publication

English

Unique Identifier

97293758

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MeSH Heading (Major)

Cholesterol|*BL; Coronary Disease|BL/DH/DT/ET/*PC; Hypercholesterolemia|BL/CO/DH/DT/*TH

MeSH Heading

Clinical Trials; Female; Human; Lipoproteins, LDL Cholesterol|BL; Male; Middle Age

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-838X

Country of Publication

UNITED STATES

Record 96 from database: MEDLINE
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Title

Cholesteryl ester transfer proteins, reverse cholesterol transport, and atherosclerosis.

Author

Bruce C; Tall AR

Address

Department of Medicine, Columbia University, New York, USA.

Source

Curr Opin Lipidol, 1995 Oct, 6:5, 306-11

Abstract

Plasma cholesteryl ester transfer protein plays a central role in lipoprotein metabolism by exchanging cholesteryl esters with triglycerides. Human genetic deficiency is associated with increased HDL-cholesterol levels, whereas cholesteryl ester transfer protein overexpression in transgenic mice results in decreased HDL-cholesterol. Thus, it has been proposed that cholesteryl ester transfer protein deficiency is an antiatherogenic state. However, recent observations in human cholesteryl ester transfer protein deficiency and cholesteryl ester transfer protein transgenic mice also suggest antiatherogenic effects of the expression of this protein, probably reflecting its role in reverse cholesterol transport.

Language of Publication

English

Unique Identifier

96047031

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MeSH Heading (Major)

Atherosclerosis|ET/*ME; Carrier Proteins|*ME; Cholesterol|*ME

MeSH Heading

Animal; Biological Transport; Cholesterol Esters|ME; Human; Lipoproteins|BL; Mice; Models, Biological

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0957-9672

Country of Publication

UNITED STATES

Record 97 from database: MEDLINE
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Title

Evaluation and management of cholesterol embolization and the blue toe syndrome.

Author

Applebaum RM; Kronzon I

Address

New York University School of Medicine, Tisch Hospital, NY 10016, USA.

Source

Curr Opin Cardiol, 1996 Sep, 11:5, 533-42

Abstract

The blue toe syndrome is characterized by tissue ischemia secondary to cholesterol crystal or atherothrombotic embolization leading to occlusion of small vessels. Embolization occurs typically from an ulcerated atherosclerotic plaque located in the aorto-iliac-femoral arterial system. Clinical presentation can range from a cyanotic toe to a diffuse multiorgan systemic disease that can mimic other systemic illness. Mortality can be higher than 70% depending on the scope of the illness. Embolization can occur spontaneously or from a variety of insults such as invasive vascular procedures, anticoagulation, or thrombolytic therapy. Angiography, duplex ultrasonography, computerized tomographic scanning, and magnetic resonance imaging have been used to image the offending lesions, with angiography considered the "gold standard" despite its inherent risks. Recently, transesophageal echocardiography has been shown to be a helpful tool in imaging the thoracic aorta and delineating in great detail the anatomy of the aortic atheroma. At present, surgery remains the most viable treatment option. However, we look to the future for large randomized trials to help predict embolization and thus the proper medical therapy.

Language of Publication

English

Unique Identifier

97044310

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MeSH Heading (Major)

Blue Toe Syndrome|*/DI/TH; Embolism, Cholesterol|*/DI/TH

MeSH Heading

Human

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0268-4705

Country of Publication

UNITED STATES

Record 98 from database: MEDLINE
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Title

Cholesterol in patients with coronary heart disease: how low should we go?

Author

Rubins HB

Address

Department of Medicine, Veterans Affairs Medical Center, Minneapolis, Minnesota 55417, USA.

Source

J Gen Intern Med, 1995 Aug, 10:8, 464-71

Abstract

CLINICAL PROBLEM: To examine the evidence supporting the recent National Cholesterol Education Program (NCEP) recommendation that low to moderate levels of cholesterol should be aggressively managed in patients with coronary heart disease (CHD). METHODS: Cohort studies and clinical trials with angiographic or clinical endpoints, that included CHD patients with low to moderate levels of cholesterol, were systematically identified through a MEDLINE search and critically reviewed. SYNOPSIS: None of the cohort studies show that a moderate level of cholesterol confers significantly increased risk of CHD death, although a pooled relative risk of 1.14 (95% CI 1.08 to 1.4) suggests that there may be a slight excess risk. Of five angiographic trials of CHD patients with moderate levels of cholesterol, two demonstrated no improvement in angiographic endpoints with intensive lipid-lowering therapy and the other three are difficult to interpret since they included other interventions in addition to the cholesterol-lowering regimen. No large clinical trial with clinical endpoints has been reported for CHD patients with low to moderate levels of cholesterol. RECOMMENDATIONS: The recommendation to treat CHD patients who have low to moderate levels of cholesterol with diet or drugs is not based on convincing evidence of efficacy. This is in clear contrast to the recommendation for CHD patients with high levels of cholesterol, for whom there is definitive clinical trial evidence of benefit from cholesterol-lowering therapy. While we await clinical trial results for CHD patients with low to moderate levels of cholesterol, clinicians and patients must consider the possible disadvantages of therapy in relation to the uncertain benefit.

Language of Publication

English

Unique Identifier

96037352

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MeSH Heading (Major)

Cholesterol|*BL; Coronary Disease|*BL/DT

MeSH Heading

Anticholesteremic Agents|TU; Clinical Trials; Cohort Studies; Female; Human; Lipoproteins, LDL Cholesterol|BL; Male; Reference Standards

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0884-8734

Country of Publication

UNITED STATES

Record 99 from database: MEDLINE
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Title

Effect of royal jelly on serum lipids in experimental animals and humans with atherosclerosis.

Author

Vittek J

Address

Department of Medicine, New York Medical College, Valhalla 10595, USA.

Source

Experientia, 1995 Sep, 51:9-10, 927-35

Abstract

The primary objective of this review was to assess the size and consistency of Royal Jelly (RJ) effect on serum lipids in experimental animals and humans. The data from animal studies were pooled, where possible, and statistically evaluated by Student's t-test. Meta-analysis was used for the evaluation of human trials. It was found that RJ significantly decreased serum and liver total lipids and cholesterol levels in rats and rabbits and also retarded the formation of atheromas in the aorta of rabbits fed a hyperlipemic diet. Meta-analysis of the controlled human trials of RJ to reduce hyperlipidemia showed a significant reduction in total serum lipids and cholesterol levels and normalization of HDL and LDL as determined from decrease in beta/alpha lipoproteins. The best available evidence suggests that RJ at approximately 50 to 100 mg per day, decreased total serum cholesterol levels by about 14%, and total serum lipids by about 10% in the group of patients studied.

Language of Publication

English

Unique Identifier

96017861

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MeSH Heading (Major)

Antilipemic Agents|*PD; Atherosclerosis|DT/*PP; Fatty Acids|*PD/TU; Lipids|*BL

MeSH Heading

Animal; Cholesterol|BL/ME; Human; Liver|ME; Rabbits; Rats

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0014-4754

Country of Publication

SWITZERLAND

Record 100 from database: MEDLINE
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Title

Cholesterol efflux from macrophages and other cells.

Author

von Eckardstein A

Address

Institute of Clinical Chemistry and Laboratory Medicine, WestfÂalische Wilhelms-UniversitÂat MÂunster, Germany.

Source

Curr Opin Lipidol, 1996 Oct, 7:5, 308-19

Abstract

Foam cell formation by lipid accumulation in macrophages is a prominent finding in atherosclerotic plaques. Since macrophages cannot limit the uptake of lipids, cholesterol efflux is probably essential to inhibit progression and cause regression of atherosclerosis. Cholesterol efflux is generally attributed to HDL in the extracellular space. Slow bidirectional fluxes of cholesterol occur between plasma membrane and lipid-rich HDL subclasses. Esterification of cholesterol in HDL by lecithin: cholesterol acyltransferase causes net cholesterol efflux. In contrast, some lipid-free apolipoproteins (especially apolipoprotein A-I) and lipid-poor HDL subclasses such as prebeta 1-apolipoprotein A-I containing lipoprotein mediate rapid and unidirectional cholesterol efflux from specific cholesterol domains in the plasma membrane. Extracellular presence of HDL or apolipoprotein A-I moreover facilitates the translocation of cholesterol from intracellular pools to the plasma membrane, probably via signal transduction. The activated transfer machinery appears to involve the Golgi apparatus and diverts cholesterol from the shuttle between acylcoenzyme A: cholesterol acyltransferase and neutral cholesteryl ester hydrolase (cholesteryl ester cycle). Endogenously synthesized apolipoprotein E facilitates HDL-mediated cholesterol efflux from macrophages. Moreover, at least in human monocyte-derived macrophages, apolipoprotein E appears to be involved in the export of cholesterol independently from extracellular acceptors. Cholesterol efflux can be inhibited by some oxysterols that are found in macrophages of atherosclerotic plaques and macrophages that are loaded in vitro with oxidized LDL.

Language of Publication

English

Unique Identifier

97091856

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MeSH Heading (Major)

Cholesterol|*ME; Macrophages|*ME

MeSH Heading

Apolipoproteins|ME; Apolipoproteins E|ME/PD; Cholesterol Esters|ME; Human; Lipoproteins, HDL|ME/PD; Receptors, Lipoprotein|ME; Sterols|ME; Support, Non-U.S. Gov't

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0957-9672

Country of Publication

UNITED STATES

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