Inflammation and heart disease

Numerous studies have shown that chronic inflammation can be the catalyst for heart disease. For decades, doctors have viewed heart disease in terms of plaque buildup and clogged arteries. Cholesterol and triglycerides were the villains. The theory was that after years of poor diet, fatty deposits or plaques would start to build up in the arteries. Eventually, this plaque would grow so large that it would cut off the blood supply to the heart, leading to angina (chest pain), high blood pressure, and, for those not treated with cholesterol-lowering drugs, a heart attack. People became concerned about their total cholesterol levels and were even able to tell the difference between low-density lipids (LDL) or bad cholesterol and high-density lipids (HDL) or good cholesterol.

Doctors militantly advocated for cholesterol levels below 200 (this number has steadily declined over the years). LDL and HDL levels became equally important. High LDL and low HDL spelled trouble. Cholesterol levels were attacked with lipid-lowering drugs (blood fats), including 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, the diagnostic images showed that the most dangerous plaques weren’t that big.

In fact, half of all those with coronary artery disease do not have any of the traditional risk factors listed above.

arterial damage

There are dozens of theories that try to explain the cause of atherosclerosis and arteriosclerosis. Scientific studies have documented the deleterious effects of elevated total cholesterol, elevated LDL, decreased 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 damage 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 is damaged by physical, chemical, viral, bacterial, or immune reactions. Once damaged, the injured tissue becomes more permeable to lipoproteins (fat transport proteins). The connective tissue of the arterial lining begins to break down, which attracts cholesterol deposits. Large white blood cells known as monocytes and blood clotting platelets stick to the injured area and cause 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 forms. The fibrous-capped plaque artroma can continue to grow until it eventually blocks blood flow through the artery. Typically, a 90 percent block is needed before symptoms of atherosclerosis are experienced.

Artromas can calcify, hardening in a process known as arteriosclerosis. Atherosclerosis of the coronary arteries can lead to thrombosis (blood clot formation), which manifests as angina (chest pain) or heart attack. Atherosclerosis of the cerebral (brain) arteries can trigger a stroke.

elevated fibrinogen

Fibrinogen is a protein involved in the regulation of blood clotting and the formation of platelet clumps.

Fibrinogen increases with 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 people with elevated fibrinogen levels were twice as likely to die of a heart attack.

Research shows that it is best to keep fibrinogen levels below 300 mg/dL.

Garlic acts as a natural blood thinner. This helps prevent clotting associated with excessive fibrinogen levels.

The recommended dosage is 4,000 mcg daily.

Fish oil supplementation helps reduce fibrinogen levels.79 The recommended dose is 4 to 9 grams per 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 to suppress excessive fibrinogen levels.

Ginkgo Biloba has over 300 clinical trials supporting 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 40 mg of ginkgo taken twice a day reduced symptoms associated with intermittent claudication (decreased circulation in the legs) by up to 45 percent.

The recommended dose is 120 mg daily.

C-reactive protein

C-reactive protein (CRP) is a marker associated with inflammation. A study published 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 of stroke.82

Elevated CRP can indicate inflammation and subsequent damage to the arterial wall which then triggers a chain reaction resulting in arteriosclerosis.

Stroke patients with the highest CRP levels were 2.4 times more likely to die in the next 12 months compared to people with the lowest CRP levels.

Vitamin C reduces C-reactive protein, blood pressure, fibrinogen levels, and Lp(a) levels.

A 10-year study revealed that more than 11,000 people who had high levels of vitamin C prolonged lifespan and reduced mortality from cardiovascular disease by 45 percent.

The recommended dose is 2 to 6 grams per day.

homocysteine

Homocysteine ​​is a byproduct of the conversion of the amino acid cysteine ​​to methionine. If homocysteine ​​is not converted to methionine, it will begin 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 binds to small LDL particles. Macrophages then break the particles and transform them into plaque.

The European Journal of Medicine reported that 40 percent of those who suffered strokes also had elevated homocysteine ​​levels compared to just 6 percent of controls.

Higher homocysteine ​​levels increased the incidence of deep vein thrombosis.

A Norwegian study involving more than 4,700 men and women showed that for every 5 millimol/L increase in blood plasma homocysteine, the number of deaths from all sources increased by 49 percent. This included a 50 percent increase in cardiovascular deaths and a 26 percent increase in cancer deaths.

Homocysteine ​​levels must be kept below 7 micromol/L of blood plasma. Laboratories generally advocate that homocysteine ​​levels be normal up to 15. However, the risk of heart attack is greatly increased when homocysteine ​​levels exceed 6.3 points.

Based on random hospital blood tests, the prevalence of elevated homocysteine ​​levels in the elderly with chronic disease is estimated to be 60 to 70 percent. Seventy percent of people with vascular disease had elevated homocysteine ​​levels. And 63 percent of those with cognitive dysfunction had elevated homocysteine ​​levels.

People 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), also known as betaine.