Atherosclerosis is a disease of the arterial intima leading to the formation of atheromatous plaques and to stenosis and occlusion of the lumen. It involves the proliferation of vascular smooth muscle cells and the accumulation of lipids. Atherosclerosis is a slow, progressive disease that may start in childhood. In some people this disease progresses rapidly in their third decade. In others it doesn't become threatening until the fifties or sixties.
Causes of Atherosclerosis
Atherosclerosis is a complex process, the precise etiology of which remains unknown. The most likely cause of atherosclerosis is oxidative damage to the endothelial layer of the artery. This causes fats, cholesterol, platelets, fibrin, cellular debris and calcium to be deposited on the arterial wall. These substances appear to stimulate the endothelial cells to produce other materials that result in further accumulation of cells on the intima, forming a lesion. These cells accumulate and many of them divide. At the same time, fat accumulates within and around the cells.
As atherosclerosis progresses, the accumulation of debris (plaque) obstructs the arterial lumen and blood flow is impacted. The end result is hypertension and increased risk of myocardial infarction, cerebral infarction and thrombosis. Gangrene may result when blood flow to the extremities is restricted.
Arteriosclerosis is due to various depositions within the plaque including lipids, cholesterol crystals, and calcium salts. These depositions cause the arteries to become rigid. The narrowing and hardening of the arteries has a significant effect on blood pressure, resistance and blood flow. Development of plaque also deforms the endothelial wall, increasing turbulent flow of blood and increasing resistance.
Platelet Derived Growth Factor (PDGF)
Platelets may also play a significant role in the development of plaque. Platelet Derived Growth Factor (PDGF) induces proliferation of fibroblasts, microglia, and smooth muscle. (The abnormal proliferation of smooth muscle cells is believed to be one of the earliest events in the process of atherosclerosis.) PDGF is released following platelet aggregation and may also serve as a chemotactic agent for inflammatory cells.
An excess of the amino acid homocysteine is a risk factor for atherosclerosis. People in the highest 25 percent of homocysteine blood level appear to be at increased risk.
Apoprotein A and Apoprotein B
Apo A is the protein component of HDL, and APO B is the protein component of LDL. Studies have shown that the ratio between APO A and APO B may be more accurate in revealing heart health than the HDL- LDL ratio.
High transferrin levels (above 50) could be indicative of hemochromatosis (abnormal iron levels). Excess iron can lead to excessive levels of oxidation within the blood vessel walls that precedes arteriosclerosis, therefore hemochromatosis is a primary risk factor for arteriosclerosis..
Atherosclerosis and Inflammation
Recently, many researchers have been examining the role played by inflammation in the development of atherosclerosis. Many now believe that there is a link between the inflammatory process and coronary atherosclerosis. One of the indications of inflammation is the presence of C-reactive protein (CRP) in the blood. Levels of this marker are elevated when heart disease is present because the plaque in diseased arteries typically contains inflammatory cells. In a survey of 388 British men aged 50-69, the prevalence of coronary artery disease increased 1.5 fold for each doubling of CRP levels*.
*Mendall MA, Patel P., Ballam L., et al. C-reactive protein and its relation to cardiovascular risk factor: A population based cross sectional study. BMJ. 1996;312:1061-1065.
It follows that reduction of inflammation within the arteries may inhibit plaque buildup and thereby reduce risk of atherosclerosis and associated heart conditions.
Laboratory Tests (Risk Assessment)
Heart attack risk can be assessed by measuring a wide range of markers, including: CRP (c-reactive protein), homocysteine, transferrin, total cholesterol, HDL and LDL, fibrinogen (a globulin that affects blood coagulation), and apolipoproteinB (apoB) and apolipoproteinA-1 (apoA-1) levels, as well as APO ratios - the higher ApoB/APO A-1 ratio may signal an increased risk of cardiovascular disease. (apoB carries LDL and VLDL cholesterol) (apoA-1 carries HDL cholesterol)
Substances that may help modify the disease process
Niacin, or vitamin B3, lowers the level of triglycerides when taken in therapeutic doses. Niacin may also lower LDL and increase HDL.
Folic acid (Folate), Vitamins B6 and B12 - Folic acid, vitamins B6 and B12 help to lower serum homocysteine levels when taken in therapeutic doses. A high quality multi vitamin mineral supplement may provide adequate doses of these B vitamins.
Omega 3 Fatty Acids such as are found in flax and hemp oil and certain cold water fish provides improved blood vessel elasticity and helps to normalize platelet function to prevent excessive adhesiveness.
Acetylsalicylic Acid -ASA- is a potent platelet inhibitor and can therefore help prevent clotting in patients who have atherosclerosis.
New opposition to aspirin therapy.
Am Heart J. 2004 Jul;148(1):157-64.
The Warfarin/Aspirin Study in Heart failure (WASH): a randomized trial comparing antithrombotic strategies for patients with heart failure.
Nutricol in Recovery is proposed to reduce inflammation in, and prevent damage to cell structures and the extracellular matrix. By reducing damage to the epithelial cells that line the arteries, the incidence and growth of atheromatous plaques is also reduced. Recovery's anti-catabolic action is proposed to protect vascular cell structures from excessive catabolism while improving anabolism. The net result is improved structure and function of vascular tissues.
Our proprietary blending of plant nutrients naturally increases the cells' receptivity to hormones such as insulin which are required to speed the repair of tissues.
Recovery contains the active ingredient Nutricol, a disease modifying anti-catabolic agent (DMAC), which Biomedica Laboratories is proud to introduce to health care professionals.
Age-related damage to the arteries associated with atherosclerosis is generally attributed to the breakdown of connective tissue within the blood vessel walls. These tissues tend to dry and become less flexible with age due mainly to:
- decreased production of fluid maintaining long-chain glycosaminoglycan structures within blood vessel walls
- decreased stability of cell membrane and extracellular collagen fibers within blood vessels and related tissues
Recovery with Nutricol is proposed to increase the structural integrity of connective tissue structures within blood vessels and maintain optimum tissue hydration. The potential results of using Recovery include:
- decreased susceptibility to blood vessel injury
- decreased catabolism of blood vessel tissues
- faster recovery rates
- decreased lactic acid buildup
- decreased inflammation and spasm
- improved blood vessel elasticity
In the treatment of atherosclerosis, Recovery is proposed to:
Reinforce membrane and matrix structures by increasing aldimine reducible cross-linking of collagen fibers; this acts to reinforce the strength and elasticity of connective tissue structures such as cartilage, synovium, ligaments, tendons, fascia, bone, blood vessel walls and the dermis of the skin.
Neutralize reactive oxygen species (ROS) and catabolic enzymes before they can negatively impact cellular and extracellular structure and function; this results in increased membrane receptivity to growth factors such as insulin, somatomedins and thyroxin that are required for anabolic repair and cellular maintenance.
Decrease catabolism of membrane and matrix collagen and glycosaminoglycan (GAG) structures via decreasing the pathological production of catabolic enzymes and other biochemicals such as collagenase, elastase, hyaluronidase, tumor necrosis factor, nitric oxide synthase and xanthine oxidase*; these biochemicals are released from immune, microbial and damaged cells and cause further damage to connective and epithelial tissue structures, resulting in joint pain, inflammation, capillary fragility and other soft-tissue damage.
Stabilize cellular membranes, preventing the release of compounds that promote inflammation such as histamine, serine proteases, prostaglandins and leukotrienes by non-competitively inhibiting the release of associated inflammatory enzymes such as cyclo-oxygenase, lipoxygenase and phosphodiesterase.
Increase the stability and production of protective epithelial mucosal surfaces in the digestive, respiratory and genitourinary tract to decrease the absorption of antigens (environmental compounds that may initiate immune or non-immune mediated inflammation, spasm and damage within blood vessels)
Biostructural Medicine goes beyond simply addressing symptoms; it is a cell structure-oriented health science that addresses the pathogenic factors of degenerative and inflammatory conditions.
Nutricol (Recovery) may be safely combined with other medications or taken on its own to help counter inflammation. It does not produce unpleasant side effects.