Plaque Attack
Heart Attacks have long been attributed to the development of plaque in artery walls. This plaque is a combination of cholesterol and calcium and usually builds up inside the artery lining cell walls. When the plaque gets large, it can either begin to block blood flow or if the covering cell membranes rupture exposing the plaque, a small piece can break off and travel in the blood stream until it reaches a narrowing vessel where it gets stuck and blocks blood flow. If the blockage is in the heart, it is called a heart attack, and if it is in the brain, a stroke.
Of Interest: Even old research, look at the year, didn't support the dietary cholesterol effect on heart disease in older people. Yet medicine did not correct the critical impression created in the media concerning cholesterol intake on mortality. ref article
This works for most heart attacks in older people, but fails to satisfy heart attacks in younger people who don't exhibit hardly any plaque build-up. This dilemma needs another explanation. The membranes do not so much tear apart as just exhibit an abrasion looking effect. ref ref
Regardless of initiation, what has to be addressed is first, why does plaque develop and can this process be modified or eliminated? Next, how can the body be protected after plaque is present to prevent rupture and clots? How might vitamins play a role? And fundamentally, is plaque build up a defensive mechanism of the body to protect the integrity of arteries once they are injured? Is the body trying to strengthen the artery wall to prevent a rupture at a damaged or injured weak spot?
These are the areas under consideration:
- Clotting ability of blood, includes Fibrinogen levels
- Thickness of blood or the stickiness or clumping of red blood cellls
- Fat profile (includes cholesterol) in blood
- Oxidation rate of fats in blood
- Artery Wall elasticity on blood pressure
- Artery wall cell membrane integrity
- inflammatory state of artery wall cells
- Markers or elements in blood related to inflammation
FACT: There are dietary nutritional vitamins, minerals, enzymes, and other phyto-nutrients in foods that have an influence over many if not all of these conditions. Magnesium> ref
IMPACT OF DIETARY CALCIUM
Here is what the Harvard newsletter says about this topic:
"Cardiovascular calcification
Calcium can accumulate in the arterial plaque that develops after an injury to the vessel wall. The plaque is usually soft to begin with, but eventually tends to harden and become calcified. In addition, blood vessel cells themselves sometimes convert into bone-forming osteoblasts, producing extra calcium on the spot. (Well! Not really producing calcium, but directing it's placement in the plaque inside the artery cell wallls).
Coronary arteries. People with arterial calcifications are more likely to develop heart disease, but it's unclear whether calcified plaque is more likely than soft plaque to rupture and cause a heart attack.
The risk of coronary artery disease can be predicted by the amount of calcium in the coronary arteries, as measured by CT scanning — even after correction for other heart disease risk factors. But the American Heart Association does not recommend these heart scans if you can tell by your medical history or other risk factors that you are at low or high risk for heart disease. If you are at intermediate risk (a 10% to 20% chance of a heart attack in the next 10 years), a coronary artery calcium scan may help your doctor determine how aggressively to pursue therapies such as statins.
If you develop chest pain, scanning for coronary artery calcium may help determine whether heart disease is the cause. Echocardiography — a procedure that uses sound waves to create moving pictures of the beating heart — may reveal calcification of the aortic valve, which greatly raises the risk for coronary artery disease.
Brain-related arteries. In most patients who undergo brain CT scans, for whatever reason, the carotid (neck) and vertebral (spine) arteries show signs of calcification. These calcifications may be an independent risk factor for stroke: a 2007 study found that calcifications are especially common in people who have had a clot-related (ischemic) stroke.
Consumption connection? Evidence is limited, but calcium intake doesn't appear to increase the risk of calcification in coronary arteries. In fact, a high level of calcium in the diet is usually thought to be beneficial to heart health, because it's associated with lower blood pressure and lower weight. However, there have been some worrisome findings.** Some studies (but not all) have found an increased risk of heart attacks among women taking calcium supplements. Researchers involved in 15 randomized trials of calcium supplements for various conditions are pooling their data on adverse events among almost 12,000 people to look for any association." -end of article copy.
Check this out, even though in Type 2 Diabetics, still some insight. Both low and high calcium intake harmful. ref
**It is now quite clear that both low and high amounts of dietary calcium increase all cause mortality and cardiovascular disease in Women. ref The safest total intake for calcium per day exhibiting the lowest mortality rate is between 600 mg and 1000 mg. This includes the amount from diet and supplements.
A Sticky Point: If the cholesterol theory was correct, one would expect to find artery damage throughout the entire artery system. BUT, damaged arteries are mainly found, or at greater degrees, at points where arteries turn or split into two channels. This generates a greater dynamic fluid turbulence leading to increased stresses on vessel walls from the blood flow. If the cells in the walls are not healthy enough, they will begin to break down or sustain an injury to the usually non-delicate membrane lining the inside of the arteries.This damaged area then prompts the body to go into a repair mode. Packing calcium and cholesterol into this damaged tissue area might simply be part of this repair attempt. Oxidized LDL is definitely a player along with inflammatory issues and these may be another source of initiation, or act as a contributer.
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