Four groups of 25 rabbits each, were studied to determine the effect of Haritaki (Terminalia chebula), Amla (Emblica officinalis) and Bahira (Terminalia belerica) on cholesterol-induced hypercholesteolaemia and atherosclerosis. The control group was fed with cholesterol alone; the Haritaki group received Haritaki and cholesterol; the Bahira group received Bahira and cholesterol; and the Amla group received Amla and cholesterol for 16 weeks.
The effect of orally administered indigenous drugs Terminalia arjuna, T. belerica and T. chebula were investigated on experimental atherosclerosis. Rabbits were fed a cholesterol-rich diet to induce atherosclerosis. The three drugs were fed along with cholesterol. At the end of the experimental period the animals were killed and their plasma and tissue lipid components estimated. Atherosclerotic lesions of the aorta were examined histologically. T. arjuna was found to be the most potent hypolipidemic agent and induced partial inhibition of rabbit atheroma. The results indicate that T.
The pathogenetic links between diet and diseases such as hypertension and atherosclerosis remain the subject of much controversy. This article reviews the evidence about the relationship between diet and these two widespread adult conditions, proposes an approach for their early recognition, examines the rationale and safety of dietary changes, and formulates specific recommendations.
Zeitschrift F¸r Die Gesamte Innere Medizin Und Ihre Grenzgebiete
Proceeding from experiences with animal-experimental studies is tried to show all those mechanisms which have influence on the ageing process of man. In these cases in the experimental part of the study is particularly investigated the influence of the restriction of food in obese patients on the cardiovascular system, the lipid metabolism and the biological age. In obese patients of middle age by isocaloric reduction diet a normalisation of the at present changed non-invasive cardiodynamic parameters could be achieved.
Current nutrition theory holds that maximization of human growth and stature is a desired anthropometric outcome. However, some evidence demonstrates that lower energy intakes may actually confer a degree of future protection against degenerative processes, particularly atherosclerosis and cancer.
Familial forms of isolated hypercholesterolemia are inherited autosomal-dominantly and are caused by defects of the low-density lipoprotein (LDL) receptor protein or its ligand, the apolipoprotein B-100, the exclusive apolipoprotein moiety of the LDL particles. Mutations at the LDL receptor gene locus (more than 150 different mutations have been described up to now) lead to familial hypercholesterolemia (FH); the only mutation at the apolipoprotein B-100 gene locus described in detail so far leads to the so-called familial defective apolipoprotein B-100 (FDB).
Lipoproteins and the impact of lipid lowering on progression and regression of coronary artery disease are discussed. Angiographically assessed regression studies are reviewed (NHLBI, LIT, LHT, CLAS I and II, FATS, POSCH, Heidelberg, STARS, SCRIP, MAAS, PLAC I, HARP, UC-SF), as are B-mode ultrasound studies (ACAPS, PLAC II) and survival studies (Oslo diet-smoking study, SSSS, Pravastatin, Oxford). Although study populations and the interventions are different in the studies, I have come to the following conclusions.
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.