How does elevated homocysteine contribute to atherosclerosis?
368598
*****Adverse vascular effects of homocysteine are modulated by endothelium-derived relaxing factor and related oxides of nitrogen.\n\nElevated levels of homocysteine are associated with an increased risk of atherosclerosis and thrombosis. The reactivity of the sulfhydryl group of homocysteine has been implicated in molecular mechanisms underlying this increased risk. There is also increasingly compelling evidence that thiols react in the presence of nitric oxide (NO) and endothelium-derived relaxing factor (EDRF) to form S-nitrosothiols, compounds with potent vasodilatory and antiplatelet effects. We, therefore, hypothesized that S-nitrosation of homocysteine would confer these beneficial bioactivities to the thiol, and at the same time attenuate its pathogenicity. We found that prolonged (> 3 h) exposure of endothelial cells to homocysteine results in impaired EDRF responses. By contrast, brief (15 min) exposure of endothelial cells, stimulated to secrete EDRF, to homocysteine results in the formation of S-NO-homocysteine, a potent antiplatelet agent and vasodilator. In contrast to homocysteine, S-NO-homocysteine does not support H2O2 generation and does not undergo conversion to homocysteine thiolactone, reaction products believed to contribute to endothelial toxicity. These results suggest that the normal endothelium modulates the potential, adverse effects of homocysteine by releasing EDRF and forming the adduct S-NO-homocysteine. The adverse vascular properties of homocysteine may result from an inability to sustain S-NO formation owing to a progressive imbalance between the production of NO by progressively dysfunctional endothelial cells and the levels of homocysteine.\n\n\n\n\n\n\n********Characterization of the stress-inducing effects of homocysteine.\n\n\nThe mechanism by which homocysteine causes endothelial cell (EC) injury and/or dysfunction is not fully understood.\n\nhomocysteine increases the expression of GRP78 and GADD153, stress-response genes induced by agents or conditions that adversely affect the function of the endoplasmic reticulum (ER). \n\nstudies indicate that the activation of stress response genes by homocysteine involves reductive stress leading to altered ER function and is in contrast with that of most other EC perturbants. The observation that homocysteine also decreases the expression of the antioxidant enzymes glutathione peroxidase and natural killer-enhancing factor B suggests that homocysteine could potentially enhance the cytotoxic effect of agents or conditions known to cause oxidative stress.\n\nPls refer to: \n\nhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=8380812&dopt=Abstract\n\nhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9576870&dopt=Abstract
202229
I'm afraid the vitamins will not affect LDL levels at all. Soluble fiber helps drop cholesterol level, as do very large doses of niacin (Vitamin B3), but vitamins E & C are anti-oxidants that help quench free radicals & they don't really do anything with cholesterol.
175605
If you can prove the answer to your question you will win a Nobel Prize!  Research is accumulating that strongly suggests that homocysteine may be harmful.  But ... it is still possible that it is merely a biomarker for methylation problems and/or other problems related to its metabolism (e.g. cysteine production).
465257
Lipitor, for high cholesterol.
612752
You have your cholesterol levels under control, but now your doctor says your triglycerides are still high. Triglycerides, like cholesterol, are blood fats. Research suggests that high levels increase risk for heart disease, diabetes, and stroke. And very high levels (see chart) put you at risk for pancreatitis, a life-threatening inflammation of the pancreas.\n\nThe good news is that lifestyle and dietary changes can significantly reduce triglyceride levels in most people. Mayo Clinic experts offer the following tips to help lower your risk of disease:\n\n* Eat fish high in omega-3 fatty acids such as salmon, mackerel, and herring.\n\n* Cut back on sugary foods, such as cookies and soda.\n\n* Cut back on alcohol.\n\n* Exercise at least 30 minutes nearly every day.\n\nThe test for triglyceride levels should be done when you are fasting and no extra triglycerides from a recent meal are present in the bloodstream. Triglyceride levels after a meal may be 10 times higher than fasting levels.
1150472
Nothing much, you just consuming extra protein. If you eat too much you will get fat or you will start to have health problems if the %% of set amino acids is over healthy set limits.
700931
Eating a high fibre diet reduces the level of bad cholesterol. eat lentils, walnuts(super healthy for the heart), an apple every night, figs,...  omega 3's like fish, nuts, avacado help increase the HDL level. Excercise definitely helps.
2723
It is a good idea to eat protein containing large amounts of arginine, such as chicken or other meats, as well as foods containing vitamin E, zinc, vitamin B6, and vitamin C.  Note however that if you have erectile dysfunction, your diet has only suble effects on this condition and will not reverse it fully unless you had a severe defficiency of some of these nutrients.
130261
Liver disease can cause high ALT, but taken together with a high alkaline phosphatase level, it is more likely a cholestatic cause, e.g., something common like gallstones can cause it too.  However, wait for the results of the tests before you jump to any conclusions.
671376
what happens in atheroschlerosis is that lipids like cholesterol get trapped into the arterial tissue, is attacked by your immune system which causes inflammation and the artery walls thicken, reducing blood flow. clots can also block arteries
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Dr Blaylock is reporting contrary to the findings of just about every other cardiologist. Current thoughts are that statins in high dosages can actually reduce ateriosclerosis, and therefore help greatly in the prevention of MI.
382429
Plasma-derived serum as a selective agent to obtain endothelial cultures from swine aorta.\n\n\n\nEndothelial cell and smooth muscle cell cultures from artery wall provide a potential model system for studying cellular processes involved in atherogenesis. To prepare serial subcultures of swine arterial endothelial cells that are free of smooth muscle cells without either selecting a small population or subjecting the cells to cytotoxic conditions, we used swine plasma-derived serum (SPDS) to establish conditions in which endothelial cells have a growth advantage. Endothelial cells were collected by collagenase digestion and smooth muscle cell cultures were prepared by outgrowth from explants of arterial medial segments. Growth rates were compared when each cell type was maintained on SPDS, or fetal bovine serum (FBS), or swine whole serum (SWS). When 20% FBS or SWS were used the doubling times were less than 30 h for both endothelial cells and smooth muscle cells. On 20% SPDS the doubling time for endothelial cells was 32 h, but for smooth muscle cells it was at least 168 h. Using SPDS, we prepare endothelial subcultures from swine aorta that express principally polygonal morphology at confluence. Endothelial cell cultures grown on SPDS have higher angiotensin-converting enzyme than those grown on FBS.\n\nBlood and serum are frequently used as samples for proteomic analysis. A consideration of the literature suggests that the differences between serum and plasma as samples are not appreciated by many investigators. There also appears to be a lack of understanding of the issues critical for the processing of plasma and serum samples for analysis. The major difference between plasma and serum is the removal of fibrinogen and associated proteins such as high-molecular weight von Willebrand factor and the variable addition of cellular secretion products as a result of the coagulation process. Factors influencing plasma quality include anticoagulant selection, processing, and storage. Factors influencing serum quality include collection container and clot retraction time. Various approaches for the removal of high abundance proteins such as albumin and immunoglobulin G will be discussed. While it is clear that the removal of these high abundance proteins provides for the analysis of otherwise obscured low-abundance proteins, studies have not been performed to document that some low-abundance proteins are also not removed by these techniques Furthermore, most studies do not have enough "normal" subjects to provide a statistically sound control value. Plasma and serum can be valuable samples for proteomic analysis but the preparation of the samples must be suitable for regulatory validation. Recommendations are presented for consideration.\n\nDoes this help?
161824
What are you measuring?\n\nIn our GC experiments, we noticed that cysteine tended to oxidize in the air. Not sure if that helps any.
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Normal values for cholesterol is from 150 mg/dL to 250 mg/dL.  so your values are still within the normal range.  Increased cholesterol from the normal range is not good for the heart and body.  How to avoid increased cholesterol values? Avoid fatty foods,( pork and chicken fat), dairy products ( cheese, butter, milk) eggs.  Exercise is also good to burn out the excess fats in your body and avoid their deposition in your adipose tissue.
47275
i think you might be eating too many vitamins that may contain b12, it's only found in meats, but ask your doc i'm not quite sure but it's fat soluable so it stores in your fat cells
320624
Artery blockage can cause high BP if blood backs up at the blockage, but it generally won't cause high BP if there's blockage just at one point. The problem is that many people with atherosclerosis (plaque buildup in the arteries) have it throughout their body, just to different degrees at different points. Atherosclerosis will result in high systolic BP (the top number of the blood pressure). Blood pressure is best treated by a combination of methods. Regular exercise (such as walking several times a week more than usual) and diet changes (eating less fatty and salty foods for example) may help blood pressure in addition to medication, but it's important to talk to your doctor about any possible changes to your blood pressure treatment.
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Cholesterol is a waxy fat like substance that is important for normal body functioning. Cholesterol is used for cellular functions and the production of hormones. Your body, in most cases, will produce enough cholesterol to maintain normal body needs. The liver is the major production factory for cholesterol (about 70%). Diets high in saturated fats, significantly increase the amount of cholesterol in the blood stream. Recommended daily intake of fat should not exceed 30% of calories, with a maximum of 10% being from saturated fat. Research indicates that diets high in saturated and total fat, play a significant role in the process of atherosclerosis (plaque build-up on the artery wall ).\n\nHigh cholesterol levels are strong indicators of those individuals that are prone to coronary heart disease. Elevated total cholesterol is a risk factor for coronary heart disease. The build-up of plaque in the artery may lead to narrowing (high blood pressure) or complete blockage (heart attack) of the vessel. As levels rise above 180 mg/dl, the risk for developing coronary heart disease increases. A cholesterol value of 220 mg/dl correlates to nearly a two-fold elevation in incidence of coronary heart disease as compared to 180 mg/dl. A reduction of 1% is shown to reduce the risk for coronary artery disease by 2% for levels over 200 mg/dl.\n\nTotal cholesterol is the sum of all the cholesterol in your blood. The higher your total cholesterol, the greater your risk for heart disease. Here are the total values that matter to you. \n\n\n\nTotal Cholesterol Levels:\n \nLess than 200 mg/dL "Desirable" level that puts you at lower risk for heart disease. A cholesterol level of 200 mg/dL or greater increases your risk. \n\n200 to 239 mg/dL  "Borderline-high."  \n\n240 mg/dL and above "High" blood cholesterol. A person with this level has more than twice the risk of heart disease compared to someone whose cholesterol is below 200 mg/dL.  \n\n\nLDL or Low density LipoProtein(Bad cholesterol) - distibute fatty deposite on vessel wall thus promotes the formation of atherosclorotic plaque.\nHDL or High Density LipoProtein(Good Cholesterol) -collects fatty deposites on vessel wall and transport to liver for bile synthesis or other metabolic activity. On this process it prevents or retards the formation of atherosclorosis. \n\nNormal Levels:\nDesirable total cholesterol: below 200 mg/dL (5.17 mmol/L) \nOptimal LDL ('bad') cholesterol: below 100 mg/dL (2.6 mmol/L) \nOptimal HDL ('good') cholesterol: over 60 mg/dL (1.56 mmol/L) \n\n\nConclusion: \nYou  have a LOW  TOTAL CHOLESTEROL level of 120 mg/dl\nImplication:\nYou are less prone to develop Coronary Artery Diseases. Good for you and keep up the healthy living.