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Hypercholesterolemias

Myocardial GSH levels are reduced within 2 weeks of cholesterol diet with a subsequent increase thereafter and this probably accounts for the different ischemic re- [Pg.57]

Milk has been cited as a possible coronary health hazard (Segall, 1977) because it contains about 3.5% of mainly saturated fat (30% palmitate, [Pg.214]

12% stearate, 28% oleate, 1.6% linoleate, and 1.0% linolenate) and about 140 mg cholesterol/1000 milliliters. On the contrary, several investigators have reported that milk is actually hypocholesterolemic in man and animals. Mann and Spoerry (1974) serendipitously discovered that consumption of large quantities of fermented milk by the Maasai tribesmen of Africa actually lowered their serum cholesterol level and counteracted the hypercholesterolemic action of Tween . It was subsequently demonstrated that unfermented milk is also hypocholesterolemic in man and animals (Richardson, 1978). In vitro and in vivo studies by Rao et al. (1981a) showed that milk fermented by Streptococcus thermophilus is hypocholesteremic and anticholesterogenic. Not all studies, however, support a hypocholesterolemic effect of dairy foods (Rossouw et al., 1981 Thompson et al., 1982). More studies are necessary to evaluate the hypocholesterolemic effect of dairy foods and to identify the hypocholesterolemic agent(s), if present. [Pg.215]


Defects in the LDL receptor have been particularly well explored as a basis of the disease familial hypercholesterolemia (93,111). A number of defects that collectively impair LDL receptor trafficking, binding, or deUvery underHe this disease where LDL and semm cholesterol rise to levels that mediate early cardiovascular mortaUty. Studies of the population distribution of this defect can determine the source of the original mutation. Thus, in Quebec, about 60% of the individuals suffering from familial hypercholesterolemia have a particular 10-kdobase deletion mutation in the LDL gene (112). This may have arisen from an original founder of the French Canadian settiement in the seventeenth century. [Pg.283]

Denke, M. A., 1995. Lack of efficacy of low-dose sitostanol therapy as an adjunct to a cholesterol-lowering diet in men widi moderate hypercholesterolemia. American Journal of Clinical Nutrition 61 392—396. [Pg.258]

A lipid lowering agent of potential value in hypercholesterolemia is cetaben (31). It is synthesized facilely by monoalkylation of ethyl -aminobenzoate with hexadecyl bromide and then saponification. " ... [Pg.60]

LDL receptor Loss-of-function (familial, autosomal dominant) Familial hypercholesterolemia (impaired clearance of LDL)... [Pg.706]

The bile acid sequestrants are used as adjunctive therapy for the reduction of elevated serum cholesterol in patients with hypercholesterolemia who do not have an... [Pg.410]

The HMG-CoA reductase inhibitors have an additive effect when used with the bile acid sequestrants, which may provide an added benefit in treating hypercholesterolemia that does not respond to a single-drug regimen. There is an increased risk of myopathy (disorders of the striated muscle) when the HMG-CoA reductase inhibitors are administered with erythromycin, niacin, or cyclosporin a When the HMG-CoA reductase inhibitors are administered with oral anticoagulants, there is an increased anticoagulant effect. [Pg.412]

Small amounts of trans-unsamrated fatty acids are found in ruminant fat (eg, butter fat has 2-7%), where they arise from the action of microorganisms in the rumen, but the main source in the human diet is from partially hydrogenated vegetable oils (eg, margarine). Trans fatty acids compete with essential fatty acids and may exacerbate essential fatty acid deficiency. Moreover, they are strucmrally similar to samrated fatty acids (Chapter 14) and have comparable effects in the promotion of hypercholesterolemia and atherosclerosis (Chapter 26). [Pg.192]

The hver and many extrahepatic tissues express the LDL (B-lOO, E) receptor. It is so designated because it is specific for apo B-IOO but not B-48, which lacks the carboxyl terminal domain of B-lOO containing the LDL receptor ligand, and it also takes up lipoproteins rich in apo E. This receptor is defective in familial hypercholesterolemia. Approximately 30% of LDL is de-... [Pg.209]

Famiiiai hyperchoiesteroiemia (type iia) Defective LDL receptors or mutation in ligand region of apo B-100. Elevated LDL levels and hypercholesterolemia, resulting in atherosclerosis and coronary disease. [Pg.228]

Familial type III hyperlipoproteinemia (broad beta disease, remnant removal disease, familial dysbetalipoproteinemia) Deficiency in remnant clearance by the liver is due to abnormality in apo E. Patients lack isoforms E3 and E4 and have only E2, which does not react with the E receptor. Increase in chylomicron and VLDL remnants of density < 1.019 (P-VLDL). Causes hypercholesterolemia, xanthomas, and atherosclerosis. [Pg.228]

Familial hypercholesterolemia (MIM 143890) Mutations in the gene encoding the LDL receptor... [Pg.432]

DAVIDSON M H, MAKI K C, KONG J C, DUGAN L D, TORRI S A, HALL H A, DRENNAN K B, ANDERSON s M, FULGONI V L, SALDANHA L G, OLSON B H (1998) Long-term effects of consuming foods containing psyllium seed husk on serum lipids on subjects with hypercholesterolemia , American Journal of Clinical Nutrition, 67, 367-76. [Pg.251]

Recent scientific studies have clearly established the nutritional role of dietary fiber in several health conditions (Jalili et al., 2000), such as hypercholesterolemia (Topping et al., 1990), diabetes (Chandalia et al., 2000) and bowel function. It is also effective in preventing urinary stones (Ohkawa et al., 1984). The Food and Nutrition Board (Institute of Medicine Report, 2001) recommended a daily allowance for fiber of 25-30 g, though it is not an essential nutrient. Rice bran fiber offers a good source of non-bloating dietary fiber and is marketed as RiceMucil by NutraStar Company in the USA. [Pg.352]

GERHARDT A L, GALLO N B (1998) Full-fat rice bran and oat bran similarly reduce hypercholesterolemia in humans. 128(5) 865-9. [Pg.372]

RUKMINI c, REDDY SASTRY c, MCPEAKP, LYNCH I (2000) Method for treating hypercholesterolemia, hyperlipidemia, and atherosclerosis. US Patent 6,126,943. [Pg.375]


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Atherosclerosis and hypercholesterolemia

Autosomal recessive hypercholesterolemia

Cardiovascular disease hypercholesterolemia

Cardiovascular diseases familial hypercholesterolemia

Children hypercholesterolemia

Cholesterol hypercholesterolemia

Endogenous Hyperglyceridemia with Essential Hypercholesterolemia

Essential Familial Hypercholesterolemia

Essential hypercholesterolemia

Familial hypercholesterolemia case report

Familial hypercholesterolemia diagnosis

Familial hypercholesterolemia lipid metabolism

Gene therapy familial hypercholesterolemia

Herbs, hypercholesterolemia

Heterozygous familial hypercholesterolemia

Homozygous familial hypercholesterolemia

Hypercholesterolemia (high blood cholesterol

Hypercholesterolemia (high blood cholesterol treatments

Hypercholesterolemia Dyslipidemia

Hypercholesterolemia Hypercholesterolemic

Hypercholesterolemia Hyperlipidemia

Hypercholesterolemia LDL receptor

Hypercholesterolemia cholesterol absorption

Hypercholesterolemia cholesterol deposition

Hypercholesterolemia diabetes mellitus

Hypercholesterolemia diet therapy

Hypercholesterolemia diseases caused

Hypercholesterolemia drugs inhibiting cholesterol synthesis

Hypercholesterolemia familial

Hypercholesterolemia familial), defective

Hypercholesterolemia familial, types

Hypercholesterolemia hypertension and

Hypercholesterolemia in children

Hypercholesterolemia isolated

Hypercholesterolemia lipoproteins

Hypercholesterolemia management

Hypercholesterolemia polygenic

Hypercholesterolemia polymorphism

Hypercholesterolemia progression

Hypercholesterolemia therapy

Hypercholesterolemia, and

Hypercholesterolemia, dietary fiber

Hypercholesterolemia, related

Hypercholesterolemia-atherosclerosis

Hypercholesterolemias, treatment

Hyperlipidemia Hypercholesterolemia Hypertriglyceridemia

In familial hypercholesterolemia

Monogenic hypercholesterolemia

Simple hypercholesterolemia

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