Atherosclerosis protective factors

Protective factors for atherosclerosis are fish oils, antioxidants, physical activity and garlic. These are discussed below. 

Liver toxicity is a rare side effect of CBZ therapy (Trimble, 1990), although a recent study reported that 9% of children on CBZ had mildly elevated aspartate aminotransferase (Camfield and Camfield, 1985). Higher mean serum total cholesterol (TC) levels, mean low-density lipoprotein level, and mean TC/high-density lipoprotein ratio have been reported in children with epilepsy treated with CBZ, compared with controls (Sozuer et ah, 1997). Conversely, an increase in serum high-density lipoproteins was reported in a smaller sample of patients treated with CBZ, and was therefore interpreted as a possible protective factor against atherosclerosis (Yalcin et ah, 1997). 

Risk and protective factors of atherosclerosis influence VCAM-1 expression [10,19]. A possible relation between VC AM expression and oxidized LDL was established when an important component of this modified lipoprotein, lysophosphatidylcholine, was shown to stimulate VCAM expression and increase adhesion of monocytes on endothelium in cell cultures [10,18,19]. Modified LDL and its constituents augment c)4 okine-activated VCAM-1 expression in human vascular endothelial cells [10,20]. In contrast, HDL inhibits cytokine-induced expression of endothelial cell adhesion molecules [10,21]. -3 Fatty acids have been found to decrease mRNA levels and surface expression of VCAM-1 in endothelial cells [10,22]. Aspirin inhibits induction of mRNA and cell surface expression of VCAM-1 by TNF-a and thereby inhibits monocyte adhesion on stimulated endothelial cells [10,23]. In contrast to ICAM-1, E-selectin, and P-selectin, endothelial VCAM-1 can mediate leukocyte adhesion via its sole interaction with the integrins 4P1 or 4P7 [10]. 

Malkin CJ, Pugh PJ, Jones RD, Jones TH, Channer KS. Testosterone as a protective factor against atherosclerosis— immunomodulation and influence upon plaque development and stability. J Endocrinol 2003 178 373-380. 

The interest in lecithin as a protective factor against heart disease arose from the finding that high ratios of cholesterol to to phospholipids in the blood were correlated with the severity of atherosclerosis." Furthermore, it is established that the phospholipids of the platelet plasma membrane play an important role in blood coagulation."... 

Cholesterol is biosynthesized in the liver trans ported throughout the body to be used in a va riety of ways and returned to the liver where it serves as the biosynthetic precursor to other steroids But cholesterol is a lipid and isn t soluble in water How can it move through the blood if it doesn t dis solve in if The answer is that it doesn t dissolve but IS instead carried through the blood and tissues as part of a lipoprotein (lipid + protein = lipoprotein) The proteins that carry cholesterol from the liver are called low density lipoproteins or LDLs those that return it to the liver are the high-density lipoproteins or HDLs If too much cholesterol is being transported by LDL or too little by HDL the extra cholesterol builds up on the walls of the arteries caus mg atherosclerosis A thorough physical examination nowadays measures not only total cholesterol con centration but also the distribution between LDL and HDL cholesterol An elevated level of LDL cholesterol IS a risk factor for heart disease LDL cholesterol is bad cholesterol HDLs on the other hand remove excess cholesterol and are protective HDL cholesterol IS good cholesterol... 

Cardiovascular disease (CVD) is one of the leading causes of death worldwide. There are a number of established risk factors including serum cholesterol levels, smoking and family history, which are responsible for between 50 and 75% of the CVD cases, with the remainder due to factors that cause atherosclerosis. Estrogen treatment such as hormone replacement therapy is known to protect against CVD by decreasing the levels of low-density... 

Some prospective and case-control studies also investigated the relationship of carotenoids and the evolution of CCA-IMT. Although the EVA study showed no association between total carotenoids and IMT, others like the ARIC study, the Los Angeles Atherosclerosis Study, " and the Kuopio Ischaemic Heart Disease Risk Factor Study demonstrated the protective role of isolated carotenoids such as lycopene, lutein, zeaxanthin, and P-cryptoxanthin on IMT. Thus, findings from prospective and case-control studies have suggested that some carotenoids such as lycopene and P-carotene may present protective effects against CVD and particularly myocardial infarcts and intima media thickness, a marker of atherosclerosis. 

Convincing evidence indicates that ROS generated both endogenously and also in response to diet and lifestyle factors may play a significant role in the etiology of atherosclerosis and CHD. Indeed, free radicals are responsible for LDL oxidation, which is involved in the initiation and promotion of atherosclerosis. Thus, protection from LDL oxidation by antioxidants such as carotenoids may lead to protection against human CHD. 

A key concept inferred from the ideas discussed above is the difference between the development of conditions that favor the clinical eruption of any form of CVD (i.e., atherosclerosis) and the proper occurrence of the clinical event, since the inductors do not necessarily have to be the same. Furthermore, the possibility exists that a concrete factor may be protective at several stages of the silent form of the disease, but once it is sufficiently advanced, it may act as a trigger. This distinction is pivotal when considering the role of hormones, which have been shown to differentially regulate atherosclerosis and proper clinical events. 

Hypercholesterolemia is well established as a risk factor for atherosclerosis. Dietary flavonoids are thought to protect against the disease by exerting hypocholesterolemic effects. However, clinical studies are not conclusive enough to provide the supporting evidence. Recent clinical studies on both normo- and hypercholesterolemic subjects with different flavonoids sources lasting 1-13... 

The polyphenols such as anthocyanidins might have a protective effect on atherosclerosis. This concept suggests that the Recommended Optimal Intake (ROI) is a more important factor for the antioxidation than the Recommended Dietary Allowance (RDA). Now, considering the absence of the appropriate methodology to identify anthocyanidins in the plasma, the analysis of the plasma antioxidant capacity might be a suitable index to define the optimal nutritional intake [95]. 

It is less likely in other forms of liver disease, such as acute hepatitis and cirrhosis. Cirrhosis may actually protect against atherosclerosis [5, 8, 9]. The reasons for this are not clear. Secondary hypercholesterolaemia frequently occurs in cholestatic conditions, but usually does not require treatment [10]. Other risk factors for hyperlipidaemia and cardiovascular disease should be assessed, as their presence may independently indicate a need for medical intervention [9]. In PBC, patients with severe, chronic disease do not appear to have an increased cardiovascular risk as a result of their hypercholesterolaemia this may be due to the presence of cirrhosis. In contrast, in less severe PBC... 

Free radical damage is considered to be a causative factor in the development of cancer and inflammatory and chronic diseases. Therefore, free radical scavenging molecules (antioxidants) may play a beneficial role in these conditions. With repect to CVD, the oxidation of low-density lipoprotein (LDL) is believed to be a critical process in the development of atherosclerosis (Berliner et al., 1995 Navab et al., 1995). The presence of oxidized LDL in the intima of an artery leads to the production of macrophage-derived foam cells, the main cell type present in fatty streaks that are believed to be the earliest lesion of atherosclerosis (Fuster, 1994). Therefore, the use of antioxidants as dietary supplements to protect against LDL oxidation may reduce both the development and progression of atherosclerosis (Gey, 1995). 

EC-SOD expression is substantially reduced in patients with coronary artery disease and appears to contribute to endothelial dysfunction in patients with this disease [188]. Overexpression of EC-SOD in vascular endothelial cells can protect against the oxidation of LDL, a major factor contributing to the development of atherosclerosis [ 189]. However, a positive correlation was found between the plasma level of EC-SOD and plasma homocysteine level (a risk... 

Pre-menopausal women suffer less cardiovascular disease than men do. This protection disappears, however, after the menopause, and hormone replacement therapy in post-menopausal women reduces cardiovascular mortality. Animal work suggests that oestrogens dilate blood vessels by an endothelium-dependent mechanism, but as yet there is no direct evidence to show that NO generation is different between men and women. This is an area of considerable interest, particularly as women have greater longevity than men and suffer less ischaemic heart disease. Abnormal NO production may occur in hypercholesterolaemia and may be related to subsequent development of atherosclerosis. There is now a body of experimental data to suggest that an abnormality in NO production or function may be causal, or at least an amplifying factor, in both hypercholesterolaemia and atherosclerosis. 

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