Numerous factors that directly contribute to endothelial dysfunction have been identified and aging individuals can easily assess their risk for vascular disease through Blood testing. The results of these blood tests can then be used to develop targeted intervention strategies to modify levels of risk factors that do not fall within an optimal range. Atherogenic factors that all aging individuals must be aware of include:
Elevated LDL cholesterol:
LDL is dangerous because it can penetrate the endothelial wall and contribute to the creation foam cells, which form the core of a plaque deposit. Oxidized LDL cholesterol (LDL that has been exposed to free radicals) within the endothelium also triggers an inflammatory process that accelerates vascular disease. We recommend keeping LDL cholesterol levels below 1.8mmol/l.
Low HDL cholesterol.
HDL protects against vascular disease by transporting cholesterol from the blood vessel wall back to the liver for disposal through a process known as reverse cholesterol transport. If HDL levels are low, then reverse cholesterol transport becomes inefficient, allowing for increased accumulation of cholesterol in the vessel wall. HDL levels of at least 1.3 to 1.6 mmol/l are recommended for optimal vascular protection.
Triglycerides interact with LDL cholesterol to form a particularly dangerous sub-type of LDL known as small-dense LDL. Small-dense LDL particles penetrate the endothelial layer and contribute to plaque formation much more efficiently than larger, more buoyant LDL particles. We recommend keeping fasting triglycerides below 1 mmol/l limit the formation of small-dense LDL particles.
The Oxidation of LDL results in severe vascular damage. Thousands of studies now reveal how oxidized LDL contributes to the entire atherogenic process from start to finish. Commercial blood tests are not yet available at affordable prices to measure oxidized LDL. Aging individuals should ASSUME their endogenous antioxidant levels (superoxide dismutase, catalase, and glutathione) are being depleted and that the oxidation of their LDL is progressively worsening. Many of the nutrient suggestions in this protocol afford considerable protection against LDL oxidation.
High blood pressure is known to aggravate endothelial dysfunction and leading researchers have identified the endothelium as an “end organ” for damage caused by high blood pressure. We suggests a target optimal blood pressure of 115/75 mmHg (or lower).
Elevated C-reactive protein.
Inflammation is central to the endothelial dysfunction that underlies vascular disease. An effective way to measure inflammation is through a high-sensitivity C-reactive protein (CRP) blood test. Studies have shown that higher levels of CRP are associated with increased risk of stroke, heart attack, and peripheral vascular disease . Stroke patients with the highest CRP levels are two to three times more likely to die or experience a new vascular event within a year than are patients with the lowest levels.
Like CRP, Lp-PLA2 is a marker of inflammation. However, Lp-PLA2 is a much more specific measure of vascular inflammation than CRP. Lp-PLA2 is an enzyme secreted by inflamed vascular plaque, thus the quantity of it in circulation correlates with the amount of inflamed plaque in the blood vessels. Levels of Lp-PLA2 above 200 ng/mL are indicative of heightened levels of vascular plaque buildup.
Elevated omega-6:omega-3 ratio.
High levels of pro-inflammatory omega-6 fatty acids relative to anti-inflammatory omega-3 fatty acids create an environment that fosters inflammation and contributes to vascular disease. It has been shown that lowering the omega-6:omega-3 ratio significantly decreases atherosclerotic lesion size and reduces numerous measures of inflammation. We recommends maintaining a blood omega-6:omega-3 ratio of less than 4:1.
High circulating levels of blood glucose (and insulin) cause microvascular damage that accelerates the atherogenic process, partly by contributing to endothelial dysfunction. It has been shown that a fasting blood glucose level of greater than 4.7 mmol/l significantly increases risk of cardiovascular related mortality. We suggests keeping fasting blood glucose levels below 4.8 mmol/ l.
As we age, we lose our ability to utilize insulin to effectively drive blood glucose into energy-producing cells. As glucose levels rise in the blood, the pancreas compensates by producing more insulin. As “insulin resistance” worsens, even more insulin is secreted in attempt to restore glucose control. Excess insulin is associated with a significantly greater risk of heart disease. Health Renewal suggests keeping fasting insulin below 5 mcIU/mL.
High homocysteine levels damage endothelial cells and contribute to the initial pathogenesis vascular disease. Homocysteine levels are associated with risk of heart disease. To keep homocysteine-induced endothelial damage to a minimum, levels of homocysteine should be kept below 7-8 µmol/L.
When a blood clot forms, fibrinogen is converted to fibrin, which forms the structural matrix of a blood clot. Fibrinogen also facilitates platelet adherence to endothelial cells. People with high levels of fibrinogen are more than twice as likely to die of a heart attack or stroke as people with normal fibrinogen levels. In a review which included data for over 154,000 patients, every 100 mg/dL increase in fibrinogen levels was associated with a significantly increased risk of developing coronary heart disease, stroke, and with vascular related mortality. This risk goes up even more in the presence of hypertension Fibrinogen levels should be kept between 295 to 369 mg/dl.
Insufficient vitamin D3.
Vitamin D protects against vascular disease via several different mechanisms, including reducing chronic inflammatory reactions that contribute to the pathology of the disease. It has been shown that low vitamin D levels are associated with increased cardiovascular mortality. Health Renewal suggests maintaining a 25-hydroxy vitamin D3 blood level of 50 – 80 ng/mL.
Insufficient vitamin K 2.
Vitamin K is essential for regulating proteins in the body that direct calcium to the bones and keep it out of the arterial wall. Low vitamin K 2 status predisposes aging humans to vascular calcification, chronic inflammation, and sharply higher heart attack risks. There is a substantial amount of evidence that suggests that supplementation with vitamin K (Ac MK-7) easily corrects the vitamin K deficits that are so common among in the first world today.
Low testosterone and excess estrogen (in men).
Numerous studies link low testosterone (and excess estradiol) with increased heart attack and stroke risk . Testosterone is intimately involved in the reverse cholesterol transport process, which removes cholesterol from the arterial wall by HDL. Excess estrogen is linked with higher C-reactive protein and a greater propensity for abnormal blood clots to form in arteries, causing a sudden heart attack or stroke. Men should keep their free testosterone in a range of 20 – 25 pg/mL and their estradiol levels between 20 – 30 pg/mL.
Supplemental CoQ10 alters the pathology of vascular diseases and has the potential for prevention of vascular disease through the inhibition of LDL cholesterol oxidation and by the maintenance of optimal cellular and mitochondrial function throughout the ravages of time and internal and external stresses. The attainment of higher blood levels of CoQ10 (> 3.5 micrograms/mL) with the use of higher doses of CoQ10 appears to enhance both the magnitude and rate of clinical improvement.
Nitric oxide deficit.
Nitric oxide is an important messenger molecule required for healthy cardiovascular function. Nitric oxide enables blood vessels to expand and contract with youthful elasticity and is vital to maintaining the structural integrity of the endothelium, thus protecting against vascular disease. Even when all other risk factors are controlled for, the age-related decline in endothelial nitric oxide too often causes accelerated vascular disease unless corrective measures are taken.