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Arteries, Blood Vessels & Plaques
Atherosclerosis; many factors involved in dead risk #1
Atherosclerosis can affect any artery in the body, including arteries in the heart, brain, arms, legs, and pelvis. As a result, different diseases may develop based on which arteries are affected.
Coronary artery disease (CAD). This is when plaque builds up in the coronary arteries. These arteries supply oxygen-rich blood to your heart. When blood flow to your heart is reduced or blocked, it can lead to chest pain and heart attack. CAD also is called heart disease, and it's the leading cause of death in the United States.
Carotid (ka-ROT-id) artery disease. This happens when plaque builds up in the carotid arteries. These arteries supply oxygen-rich blood to your brain. When blood flow to your brain is reduced or blocked, it can lead to stroke.
Peripheral arterial disease (PAD). This occurs when plaque builds up in the major arteries that supply oxygen-rich blood to the legs, arms, and pelvis. When blood flow to these parts of your body is reduced or blocked, it can lead to numbness, pain, and sometimes dangerous infections.
Some people with atherosclerosis have no signs or symptoms. They may not be diagnosed until after a heart attack or stroke.
The main treatment for atherosclerosis is lifestyle changes. You also may need medicines and medical procedures, however there are very large numbers of dangerous side effects involved. Statins are the #1 selling drug with sales over 25.000.000.000 US$ anually. Almost impossible to get objective information.
The cause of atherosclerosis isn’t known. Many recent studies show into the direction of the lack of vitamin K2 and D3. However, more conditions may raise your chances of developing it. These conditions are known as risk factors. You can control most risk factors, such as lack of physical activity, smoking, and unhealthy eating. Others you can’t control, such as age and family history of heart disease. The last two however are minor factors of risk. Atherosclerosis doesn't develop because of age but because of life style.
Better treatments have reduced the number of deaths from atherosclerosis-related diseases. These treatments also have improved the quality of life for people with these diseases. Still, the number of people diagnosed with atherosclerosis remains high.
You may be able to prevent or delay atherosclerosis and the diseases it can cause, mainly by maintaining a healthy lifestyle and using food or supplements rich in Vitamin K2 and D3, along with resveratrol, polyphenols such as green tea, omega 3 fatty acids and many more nutrients and antioxidants. This, along with ongoing medical care, can help you in avoiding the problems of atherosclerosis and live a long, healthy life.
The clinical and experimental research of metabolic effects of shark liver oil
Biochem Biophys Res Commun. 2001 Nov 30;289(2):485-90. Vopr Pitan. 2007;76(6):28-Pogozheva AV, Derbeneva SA, Anykina NV, Kondakova NM, Kulakova SN, Medvedev FA, Mal'tsev GIu, Trushina EN, Mustafina OK, Pozdniakov AL, Gadzhieva ZM.
The investigation of influent of antiatherosclerotic diets with shark liver oil on clinical and metabolic parameters in patients with cardiovascular diseases. Results of the study show that enrichment of a diets with shark liver oil in patients with ischemic heart disease and hypertension improved clinic status, antropometric levels, lipid spectrum of blood and immunology status. The mechanism of shark liver oil was investigated in rats.
Matrix Gla protein accumulates at the border of regions of calcification and normal tissue in the media of the arterial vessel wall.
Biochem Biophys Res Commun. 2001 Nov 30;289(2):485-90. Spronk HM, Soute BA, Schurgers LJ, Cleutjens JP, Thijssen HH, De Mey JG, Vermeer C.
Department of Biochemistry, Maastricht University, Maastricht, The Netherlands.
Vitamin K-dependent matrix Gla protein (MGP) has been suggested to play a role in the inhibition of soft-tissue calcification. Here we report the expression of recombinant prokaryotic MGP as part of a fusion protein and the preparation of two antibodies that specifically recognize MGP. Monoclonal antibodies were raised against synthetic peptides homologous to the sequences 3-15 and 63-75 of human MGP. Both antibodies recognize recombinant and synthetic human MGP. Immunohistochemical analysis showed that MGP was associated with the extracellular matrix of noncalcified bone and with chondrocytes in cartilage. In the healthy human arterial vessel wall, MGP antigen was demonstrated in association with smooth muscle cells and elastic laminae of the tunica media and with the extracellular matrix of the adventitia.
Colocalization with the elastic laminae was lost at sites of medial calcification; in both human and rat arteries, high amounts of MGP were found in the extracellular matrix at borders of intimal and medial calcification. Our data demonstrate the close association between MGP and calcification. It is suggested that undercarboxylated MGP is biologically inactive and that poor vascular vitamin K status may form a risk factor for vascular calcification.
Elastogenic effects of exogenous hyaluronan oligosaccharides on vascular smooth muscle cells.
Joddar B, Ramamurthi A.Biomaterials. 2006 Nov;27(33):5698-707. Epub 2006 Aug 8.Department of Bioengineering, Clemson University, Charleston, SC 29425, USA.
Prior studies suggest that hyaluronan (HA), a glycosaminoglycan, may upregulate innately poor elastin matrix synthesis by adult vascular smooth muscle cells (SMCs). HA scaffolds could thus be useful to regenerate damaged vascular elastin. In an earlier study, we established that the elastogenic effects of non-oligomeric HA are fragment size- and/or dose-specific. We currently investigate the pro-elastogenic effects of exogenous HA oligomers on rat aortic smooth muscle cells (RASMCs). RASMCs were cultured with pure HA oligomers (4-mers) and mixtures (4-8mers) obtained by enzymatic digestion of long-chain HA (MW approximately 2000kDa).
Polyacrylamide gel electrophoresis (PAGE)/Matrix Assisted Laser Desorption/Ionization Spectroscopy Time-Of-Flight Analysis (MALDI-TOF) showed HA digestates to contain a mixture of 4-8mers with a predominance of 4-mers (75+/-0.4% w/w). Cell layers supplemented with both pure HA 4-mers or oligomer mixtures showed proliferation levels similar to non-HA controls over 21 days of culture.
Pure 4-mers and oligomer mixtures enhanced DNA-normalized output of tropoelastin by 1.6 and 1.8 times, respectively, and that of matrix elastin by approximately 2.7 times relative to controls. Sodium dodecyl sulfate (SDS)-PAGE/Western Blot and a desmosine assay semi-quantitatively confirmed the observed biochemical trends for tropoelastin and matrix elastin, respectively. HA oligomers induced enhanced synthesis of the elastin crosslinker, desmosine, and appeared to stabilize the elastin matrix by suppression of elastin-laminin receptor (ELR) activity relative to controls.
Transmission electron micrographs (TEMs) showed elastin deposits within oligomer-supplemented cultures to be distinct, longitudinally oriented, aggregating fibrils, and clumps, and to be less abundant and mostly amorphous in controls. HA oligomers preserved normal fibrillin-mediated elastin matrix deposition. Results suggest that HA oligos are highly pro-elastogenic, promote elastin fibril formation, and stabilize elastin matrix and may thus be usefully incorporated into scaffolds for guided elastin regeneration.
Atherosclerosis is a type of arteriosclerosis, and is one of the leading causes of illness and death in the United States. It involves the thickening and hardening of arteries, and usually affects large and medium-sized arteries. The process may begin in childhood and often progresses when people grow older. The damage begins in the innermost layer of the artery or endothelium.
Elevated plama oxidized cholesterol and triglyceride levels, high blood pressure, diabetes, and tobacco smoke are major risk factors for arterial wall damage. Plaques (fats, cholesterol, platelets, cellular waste products, calcium and other substances) are deposited in the damaged endothelium. These deposits further stimulate the cells in the artery walls to produce factors that promote the proliferation of smooth muscle cells and the accumulation of lipids. Also medicine like warfarin or coumarin speed up the calcification of the arteries. As a consequence, artery's diameter may shrink, resulting in disturbances in blood flow and oxygen delivery to tissues.
The complications of atherosclerosis include CVA, HTN, CAD, mesenteric ischemia, and/or peripheral vascular disease. Treatment should be individualized with the identification of specific risk factors. Lifestyle modification (e.g., exercise and diet) should be encouraged.
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