Numerous studies have shown that chronic inflammation may be the catalyst for heart disease. For decades doctors have viewed heart disease in terms of plaque build up and clogged arteries. Cholesterol and triglycerides were the villains. The theory was that years of poor diet fatty deposits or plaques would start to build up with in the arteries. Eventually this plaque would grow so large that they would cut off the blood supply to the heart resulting in angina (chest pain), high blood pressure, and for those left untreated with cholesterol lowering drugs, a heart attack. People began to be concerned about their total cholesterol levels and could even tell the difference between low-density lipids (LDL) or bad cholesterol and high-density lipids (HDL) or good cholesterol.
Doctors militantly advocated cholesterol levels below 200 (this number has steadily dropped over the years). The LDL and HDL levels became just as important. A high LDL and a low HDL spelled trouble. Cholesterol levels were attacked with lipid (blood fats) lowering drugs including the statins- Lipitor, Zocor, Crestor, Vytorin, and others.
However, there is a problem with this script. Half of all heart attacks occur in people with normal cholesterol levels! And to their surprise diagnostic imaging showed that the most dangerous plaques were not that large.
In fact half of all those who have coronary artery disease do not have any of the traditional risk factors as mentioned above.
There are dozens of theories, which attempt to explain the cause of atherosclerosis and arteriosclerosis. Scientific studies have documented the ill effects of total cholesterol, elevated low-density lipids (LDL), decreased high-density lipids (HDL), homocysteine, fibrinogen, oxidative stress, elevated C-Reactive Protein (CRP), inflammation, sedentary lifestyles, diabetes, obesity, infections, and stress.
The most widely accepted theory is based on the idea that injury to the arterial wall from the list above (inflammation, high blood pressure, elevated LDL, etc) initiates physiological changes that then create atherosclerosis.
The endothelial lining of the artery becomes damaged from physical, chemical, viral, bacterial, or immune reactions. Once damaged, the injured tissue becomes more permeable to lipoproteins (fat-carrying proteins). The arterial linings connective tissue begins to breakdown, which attracts cholesterol deposits. Large white blood cells known as monocytes and blood clotting platelets attach themselves to the injured area causing plaque to form.
A fibrous cap (consisting of collagen, elastin and glycosaminoglycans) forms over the injured area. Cholesterol and fat begin to build-up around the site and an arthroma is formed. The arthroma of fibrous coated plaque may continue to grow until it eventually blocks the flow of blood through the artery. It usually takes a ninety percent blockage before the symptoms of atherosclerosis is experienced.
Arthromas may calcify, hardening in a process known as arteriosclerosis. Atherosclerosis of the coronary arteries may lead to thrombosis (blood clot formation), which manifests itself as angina (chest pain) or a heart attack. Atherosclerosis of the cerebral (brain) arteries may trigger a stroke.
Fibrinogen is a protein that is involved in regulating blood clotting and platelet clumping.
Fibrinogen is increased by inflammation, oxidative damage, smoking, stress, oral contraceptives, and aging.
Elevated fibrinogen levels have also been shown to increase the incidence of stroke.
The New England of Medicine reports that those with elevated levels of fibrinogen were than twice as likely to die of a heart attack.
Research shows that it is best to keep fibrinogen levels below 300mg / dl.
Garlic acts as a natural blood thinner. This helps prevent the clotting associated with excess fibrinogen levels.
Recommended dose is 4,000 mcg a day.
Fish oil supplementation helps to reduce fibrinogen levels.79 Recommended dose is 4-9 grams a day.
Curcumin is the yellow pigment found in turmeric. It is a powerful antioxidant with potent anti-inflammatory properties. Curcumin's ability to reduce inflammation helps squelch excess fibrinogen levels.
Ginkgo Biloba has over 300 clinical trials that support its use in the management of cardiovascular and cognitive disorders. Ginkgo acts as a vasodilator to lower blood pressure, improve blood flow to the extremities (legs), and reduces fibrinogen levels.
One study showed that 40mg of ginkgo taken twice a day reduced the symptoms associated with intermittent claudication (decreased circulation to the legs) up to 45 percent.
Recommended dose is 120mg a day.
C-Reactive protein (CRP) is a marker associated with inflammation. A study reported in the New England Journal Medicine found that CRP is a strong predictor of heart attack and stroke. Men with the highest percentage points had three times the risk of heart attack and twice the risk for stroke.82
Elevated CRP may indicate inflammation and subsequent arterial wall damage that then sets off a chain reaction resulting in arteriosclerosis.
Stroke patients with the highest CRP levels were 2.4 times more likely to die with in the next 12 months compared to individuals with the lowest levels of CRP.
Vitamin C lowers C-reactive protein, blood pressure, fibrinogen levels, and Lp (a) levels.
A 10-year study revealed that the 11,000 plus individuals who had high levels of vitamin C extended lifespan and reduced mortality from cardiovascular disease by 45 percent.
Recommended dose is 2-6 grams a day.
Homocysteine is a byproduct of the conversion of the amino acids cysteine into methionine. If homocysteine is not converted into methionine it will start to accumulate in the endothelial cells of the arterial wall. This leads to plaque formation and possible arterial occlusion. Homocysteine speeds up the oxidation (causing toxic damage) of cholesterol, which then becomes bound to small LDL particles. Macrophages then the particles and transform them into plaque.
The European Journal of Medicine reported that 40 percent of those who had strokes also had elevated homocysteine levels compared to only 6 percent of controls.
Higher levels of homocysteine increased the incidence of deep vein thrombosis.
A Norwegian study involving over 4700 men and women showed that for each 5-millimol / L increase in homocysteine blood plasma caused the number of deaths from all sources to jump to 49 percent. This included a 50 percent increase in cardiovascular deaths and a 26 percent increase in cancer deaths.
Homocysteine levels should be kept below 7micromol / L of blood plasma. Laboratories general advocate that homocysteine levels are normal up to 15. However, the risk of heart attack greatly goes up when homocysteine levels go above 6.3 points.
Based on random hospital blood tests the prevalence of elevated homocysteine in the elderly with chronic illnesses is estimated to be at 60-70 percent. Seventy percent of those with vascular disease had elevated homocysteine levels. And 63 percent of those with cognitive dysfunction had elevated homocysteine levels.
Individuals with elevated homocysteine levels should supplement with 500-800mcg of folic acid, 1000-3000mcg of B12, 100-259mg of B6, and if needed 500-900mg of trimethylglycine (TMG) otherwise known as betaine.