Cardiovascular disease causes 1 of every 2.7 deaths in the United States today.1
Unless a drastic change occurs in the way doctors treat vascular disorders, aging adults face even greater threats of heart disease and stroke.
Mainstream doctors keep trying to find simple answers to protect against atherosclerotic disease. The problem is that scientists have identified at least 13 different factors that all conspire to destroy our aging arteries.
The illustration below depicts 13 named daggers aimed at the heart. Any one of these daggers can trigger a cardiovascular event, yet conventional medicine pretends that guarding against only a few of these proven risk factors adequately prevents vascular disease.
By failing to comprehend the underlying processes involved in circulatory breakdown, most doctors overlook documented methods of maintaining healthy blood flow in our maturing bodies.
In my early career, I performed over 300 postmortem arterial dissections. In aged cadavers, I often found arteries that were so occluded that it was virtually impossible to insert a small catheter (tube) into them. My experience provided a vivid image of the jagged structural devastation inflicted by atherosclerosis.
As you will read, many of today’s physicians seem to have forgotten what they should have observed in medical school. The result is a misconception of epidemic proportion that threatens the lives of tens of millions of aging Americans.
Cardiologists Still Don’t Get It
Mainstream medicine is fixated on the misconception that atherosclerosis is caused by excess levels of “lipids” in the blood. Lipids are usually defined as total cholesterol, LDL (low-density lipoprotein), and triglycerides, though other fatty substances contribute to the atherosclerotic process.
What doctors fail to understand is that atherosclerosis begins when the inner arterial wall (the endothelium) sustains an injury.2 Endothelial injuries are caused by numerous and often unavoidable factors. As humans age (and engage in bad habits), the endothelium becomes progressively dysfunctional. The end results are the major structural changes clinically defined as “atherosclerosis.”
People often analogize atherosclerosis as a “clogged pipe.” When a “clog” occurs in a coronary artery, the recommendation is either bypass surgery or a procedure in which a stent is inserted to keep the artery open. While these surgical procedures have become necessary for many people, the “clogged pipe” analogy is an inaccurate way to view the atherosclerosic process.
The underlying reason why arteries become occluded in older people is the progressive deterioration of the endothelial lining (the inner arterial wall). If people do not take steps to correct the “endothelial dysfunction” occurring in their aging bodies, the consequence will be a worsening epidemic of arterial disease that currently kills 37% of all Americans and 30% of people worldwide.3
Daggers Aimed at Your Arterial Wall
If one accepts the premise that age-related arterial disease is almost universally caused by “endothelial dysfunction,” then human studies in which a single agent is tested to prevent heart attack or stroke begin to look absurd, at least in those who seek to maintain healthy blood flow over the long term.
High blood pressure,4-10 excess cholesterol-LDL-triglycerides,11-20 low HDL,21-23 cigarette smoking,24-32 diabetes,33-38 obesity,39-42 and lack of exercise43-49 all contribute to endothelial dysfunction and the subsequent development of atherosclerosis.
Additional endothelium-damaging factors include high-normal levels of glucose,50-52 insulin,53,54 iron,55-57 homocysteine,58-84 and fibrinogen,85-98 low free testosterone (in men),99-102 and any level of C-reactive protein that is higher than optimal.103-125
Homocysteine causes initial injury to the endothelium, contributes to the production of pro-inflammatory cytokines, and facilitates the oxidation of the fat/LDL that accumulates beneath the damaged endothelium. Homocysteine also increases the expression of adhesion molecules and the abnormal accumulation of blood components around the atherosclerotic lesion.
Fibrinogen is a clotting factor that accumulates at the site of the endothelial lesion, contributing to plaque buildup. Fibrinogen can also participate in the acute blockage (thrombosis) of an artery after unstable atherosclerotic plaque ruptures.
Glucose at even high-normal levels may accelerate the glycation process that causes arterial stiffening, while high-normal fasting insulin inflicts direct damage to the endothelium and induces abnormal platelet aggregation.
High levels of iron promote oxidation of LDL in the damaged endothelium, while low levels of testosterone appear to interfere with normal endothelial function. Low levels of vitamin K enable calcium to be deposited into atherosclerotic lesions, instead of into the bone where it belongs.126-129
C-reactive protein is an inflammatory byproduct that directly damages the endothelium. This not only creates initial injuries to the endothelium, but also accelerates the progression of existing atherosclerotic lesions.
Nitric oxide is produced in the endothelium and regulates endothelial cell interactions, arterial wall blood flow, vascular tone, and platelet aggregation-adhesion. Abnormalities in nitric oxide production are a direct cause of endothelial dysfunction, which is the prelude to atherosclerosis (and often hypertension). The common feature of endothelial dysfunction is a decrease in the amount of nitric oxide.130
In response to overwhelming published data, health-conscious people are altering their diets, taking drugs, hormones, and dietary supplements, and even trying to exercise in order to reduce all of these known atherosclerosis risk factors. Despite these efforts, protecting against these risk factors until now has been only a partial solution.
One problem is that age itself is a major risk factor for endothelial dysfunction and subsequent atherosclerosis. Fortunately, there are now proven ways to protect against the many risk factors (i.e., all 13 daggers) that are the underlying causes of today’s heart attacks and strokes.
Differing Views on Homocysteine
Homocysteine is one of many factors involved in the atherosclerotic process. A recent analysis of some previous studies using folic acid in patients with preexisting cardiovascular disease claimed that this vitamin provided no benefit. A major flaw in this analysis is that none of the actual studies cited in this review lowered homocysteine levels enough to meaningfully reduce cardiovascular risk.131
Based on published epidemiological data, homocysteine should ideally be below 7-8 µmol/L of blood in order for homocysteine to no longer be a risk factor for vascular disease.132,133 Table 1 below represents the before and after homocysteine blood levels in 11 studies that were used to erroneously discredit the dangers of homocysteine.133-143
As can be clearly seen in Table 1, in none of these studies was homocysteine adequately reduced to safe ranges of below 7-8 µmol/L of blood. As is also shown in the table, some groups with severely high homocysteine had levels that remained very high even after folic acid supplementation. In other groups, homocysteine levels were not particularly high to begin with, suggesting that the preexisting vascular disease in these study subjects may have been caused by one or more of the 12 other proven risk factors (daggers).
These hard facts did not stop the media from proclaiming that those with preexisting vascular disease were wasting their money by taking folic acid supplements. None of these studies, by the way, evaluated the effects of folic acid supplementation on healthy people.
Even if homocysteine had been sufficiently lowered, it is doubtful that significant benefits would have been observed—the reason being that people with “preexisting” cardiovascular disease already suffer arterial damage that is so severe that far more than a folic acid supplement is needed to restore healthy blood flow.
Remember the 13 correctable risk factors (daggers) involved in arterial degradation and occlusion shown on the first page of this article. It is ludicrous to think that mitigating one risk factor (such as homocysteine) would result in some miraculous benefit in people already afflicted with massive damage to their inner arterial wall (i.e., endothelial dysfunction).
Based on the disparaging attacks made by mainstream cardiologists against folic acid, it is obvious that these doctors remain in a pathetic state of ignorance regarding why so many of their patients suffer from chronic circulatory disorders.
At the same time the negative review on homocysteine was released, another published scientific review came to very different conclusions about the role that homocysteine plays in a host of age-related disorders.144 Needless to say, the media ignored the paper that advised aging humans to lower toxic homocysteine levels.