Atherosclerosis is perhaps the single most deadly disease in all western countries. The most common symptoms are chest pain, shortness of breath, cognitive impairment and leg pains. If the atherosclerotic plague deposit ruptures the symptoms are usually acute and often in the form of a heart attack, stroke or embolism.
The cause and progression of atherosclerosis is related to the health of the inner arterial wall endothelial cell lining. When this inner endothelial wall lining is damaged it is referred to as endothelial dysfunction. This damage to the inner wall lining causes it to become leaky and thus allows lipids and toxins to penetrate through into the outer smooth muscle cells of the arterial wall lining. In response, the endothelium signals white blood cells to congregate along the cell wall which then produce inflammatory substances which creates inflammation. Cholesterol and triglycerides accumulate at the damaged site and become oxidized. The smooth muscle cells also produce collagen to repair the injury. This mixture of oxidized lipids, white blood cells, collagen and calcium forms a plague deposit. If this plague deposit ruptures a blood clot can form which results in a heart attack or stroke.
Risk factors which aggravate the plague formation process described above include:
(1) Smoking and obesity
(2) Diabetes/Insulin resistance – high levels of circulating sugars cause microvascular damage to endothelial cells, via glycation, which causes inflammation and acceleration of the atherosclerotic process. One way to indirectly measure the glycation process is to measure Haemoglobin A1c, which is the glycosylated form of haemoglobin.
(3) LDL cholesterol – this oxidized form of cholesterol is dangerous because it penetrates the endothelial wall forming the core of the plague deposit, in addition to triggering inflammation which accelerates the process.
(4) C Reactive Protein (CRP) – Inflammation is central to endothelial dysfunction which underlies cardiovascular disease. One way to measure inflammation is through CRP. Studies have shown higher levels of CRP increase the risk of heart attack, stroke and peripheral vascular disease.
(5) Homocysteine – contributes to inflammation and the production of free radicals that attack endothelial cells stimulating the plague formation. High homocysteine levels are also responsible for the oxidization of cholesterol to the LDL form which can then irritate artery walls leading to plague build up. In addition homocysteine reduces the flexibility of your arteries by two different mechanisms. (1) by damaging the artery lining which then begin to stiffen as a result, (2) by directly reducing nitric oxide levels which is required by the arteries to relax and remain flexible. Some studies show that high homocysteine levels increase your risks of heart attack and stroke by as much as 70%. Despite the evidence far too few doctors are testing for homocysteine and reducing it when found to be excessive. The American heart Association published a paper which indicates that levels above 6.3 increases the risk of cardiovascular disease, however the risk increases as homocysteine levels increase further.
(6) Fibrinogen – is involved in the blood clotting process and facilitates platelets adhering to endothelial cells. People with high fibrinogen are twice as likely to die of a heart attack or stroke when compared to those with normal levels. In a study to determine the relative risk of elevated fibrinogen on disease, compared to other risk factors such as cholesterol and C-Reactive Protein (CRP), scientists in London conducted a prospective study on over 3,000 patients with angina pectoris. The scientists found that if fibrinogen levels were low, even highly elevated levels of cholesterol and/or C-reactive protein presented little risk of heart attacks. However, high levels of fibrinogen in combination with low-moderate levels of cholesterol presented a significant risk.
(7) High Lipoprotein A -Lp (a) has a direct impact on the development of atherosclerosis. It is able to bind to fibrin clots in the injured arterial endothelium and, therefore, deliver cholesterol to that region in order to heal the wound. In this way, it contributes to the formation of fatty plaques. Lipoprotein(a) is a 10 times more dangerous risk factor than Low Density Lipoprotein or cholesterol.
(8) High Blood Pressure.
(9) Living in Contraction – In order to treat the whole being not only should the physical aspect be addressed but also the underlying energetic/emotional factors which also contributes equally towards developing cardiovascular disease. This includes not expressing love, not truly letting love and others in and holding back from expressing who we truly are which is usually out of fear of how others may react to it. These behaviors cause our cardiovascular system to contract and harden thus causing cardiovascular issues.
Unfortunately many physicians have a fixation on only cholesterol being a major cause of heart disease which defies the last 15 years of science and deflects from the other major factors mentioned above. Cholesterol is not the only culprit for cardiovascular disease as the pharmaceutical companies that produce billion dollar cholesterol medication every year would like you to believe. If cholesterol is oxidized to the LDL form it can irritate/inflame tissues such as the lining of our arteries but this does not mean that you should avoid cholesterol at all costs but rather we should avoid its oxidation. In fact, cholesterol is being transported to tissues as part of an inflammatory response that is there to repair damage. When damage is occurring and inflammation is being initiated, chemicals are being released so that that damage can be repaired. One could speculate that to replace damaged, old and worn-out cells the liver needs to be notified to either recycle or manufacture cholesterol since no human cell can be made without it. In this case, cholesterol is being manufactured and distributed in your bloodstream to help you repair damaged tissue.
If excessive damage is occurring such that it is necessary to distribute extra cholesterol through the bloodstream, it would not seem very wise to merely lower the cholesterol and forget about why it is there in the first place. It would seem much smarter to reduce the extra need for the cholesterol by avoiding the excessive damage that is occurring to begin with. In addition cholesterol is required by the body for many other important processes, such as hormone production and new cell formation, and if levels are maintained too low they all begin to suffer as a consequence which will ultimately lead to poor health. Like all things in the body an ideal amount is required for optimal physiological function which should be maintained without excluding the many other important factors required for good cardiovascular health.
Any program aimed at reducing the risks of cardiovascular disease, or slowing the progression of atherosclerosis, must begin with comprehensive blood testing. The tests we recommend include:
(1) Homocysteine – Ideally should be less than 6.
(2) CRP – Ideally should be less than 1.
(3) Fibrinogen – Ideally should be less than 300mg/dL
(4) Haemoglobin A1c – Ideally less than 6%.
(5) Cholesterol – Ideally should be between 3.9 to 5.5 mmol/L
(6) LDL – Ideally below 2.0mmol/L.
(7) Triglycerides – Ideally below 1.5mmol/L
(8) Lipoprotein A – ideally less than 35nmol/L
If any of these parameters are found to be higher than the ideal value then action needs to be taken to reduce their levels back into the safe range thus reducing your risk factors for heart disease.
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