Atherosclerosis

Negative attitudes such as anger, hostility, distrust, depression and anxiety are often contributing factors.

The authors of one study state, "This... study suggests that high hostility levels may contribute to early subclinical atherosclerotic coronary artery disease."  According to background information in the study, hostility is a personality and character trait with attitudinal (cynicism and mistrust of others), emotional (anger) and behavioral (overt and repressed aggression) components. [Journal of the American Medical Association. 2000; 283: pp.2546-51]

Numerous studies have confirmed premature, accelerated atherosclerosis in SLE patients.  Although the exact cause is not known at this point, atherosclerotic heart disease is a common cause of morbidity and death amongst lupus patients.

Peripheral artery disease is a likely sign of more widespread accumulation of fatty deposits in your arteries: Atherosclerosis of the peripheral arteries is by far the most common cause of peripheral vascular disease.

Hardening of the arteries (atherosclerosis) weakens artery walls and predisposes the damaged portion to enlargement.

Atherosclerosis is a risk factor for reduced circulation in the brain, sometimes called ischemic vascular dementia (IVD).

Tobacco smoke contains more than 4,000 chemicals, more than 50 of which have been identified as carcinogens.  These chemicals are extremely damaging to the cardiovascular system.  Specifically, these chemicals are carried in the bloodstream on LDL cholesterol, where they either damage the lining of the arteries directly or they damage the LDL molecule which then damages the arteries.  High cholesterol levels compound the risks.

Excessive platelet aggregation has been linked with the development of atherosclerosis and other cardiovascular conditions.

Excessive sugar consumption has been linked to elevated triglycerides and may contribute to atherosclerosis, especially in individuals with elevated insulin levels.

Low estrogen levels raise LDL-C (bad) cholesterol, while lowering HDL (good) cholesterol, both of which contribute to atherosclerosis.  Supplemental estrogen reduces this risk, at least partially by increasing the HDL particle size which confers some protection against heart disease.

Researchers at Columbia University Medical School found that serum testosterone levels were about 90ng/dl lower in patients who had suffered myocardial infarctions (MI) than in those who had not.  These results suggest that low testosterone levels predispose men to MI and are lower in men with severe coronary artery atherosclerotic disease than in controls.

Although there is some conflicting evidence, many researchers conclude that maintaining normal levels of DHEA provides some protection against atherosclerosis.

LDL is the cholesterol type most commonly thought of as a strong risk factor for atherosclerosis and heart disease.  Oxidized LDL and the fraction called Lp-a produce a greater risk.  Since HDL cholesterol reduces the risk, low HDL levels are not desirable.

Multiple studies indicate that 15-30% percent of patients with premature occlusive vascular disease have moderately elevated total plasma homocysteine concentrations. [ JAMA 1992; 268: pp.877-81]

Depression is emerging as a risk factor for heart disease.  A study of 688 women showed that depression and anger are associated with hardening of the arteries in women, in part through physical and behavioral risk factors such as bad cholesterol levels, obesity and smoking. [Psychosomatic Medicine, March/April 2001]

Researchers conclude that chronically high levels of anxiety are a risk factor for the progression of atherosclerosis, especially in men. [Arterioscler Thromb Vasc Biol 2001; 21: pp.136-41]

Manganese strengthens arterial tissues, making them more resistant to plaque formation.

Experimental studies have demonstrated a correlation between magnesium deficiency and atherosclerosis, but without any clear evidence to determine the mechanisms involved.  Magnesium deficiency may affect the atherosclerosis process through several different mechanisms.

While there has been much emphasis on low fat diets, there are some intriguing studies that show that a low fat diet may actually increase LDLs and that it may be more important to alter the fats in the diet, decreasing saturated fats and trans fatty acids, and replacing them with poly- and mono-unsaturated fats.  Hydrogenated oils are at least, if not more, atherogenic than saturated fats.

The vegetarian diet promotes stabilization or possible reversal of the atherogenic process.

Circulation, the journal of the American Heart Association, reported on a study that has correlated the degree of carotid arterial atherosclerosis with exaggerated response to mental stress in men under the age of 55.  Patients whose blood pressure responses to stressful situations were the strongest were found to have significantly more advanced atherosclerosis in the carotid arteries than those whose blood pressure responses were less pronounced.

Although researchers are careful not to say that stress causes atherosclerosis, the evidence clearly points to cardiovascular reactivity to stress as an atherosclerotic risk factor of the same magnitude as smoking, hypertension, insulin resistance, and elevated cholesterol levels.  The hypothesis is that "Frequent and prolonged periods of elevated blood pressure during mental stress may promote mechanical injury to the endothelial lining or cause release of hormones that can promote the build up of plaque." [Circulation Vol. 96, No. 11: pp.3842-48]

Moscow scientists stated in October, 2000 that they have shown atherosclerotic plaques in blood vessels are formed because of adrenaline, a hormone that releases during stress.

High-potency antioxidant supplements can reduce atherosclerosis in humans.  A study involving 11,178 elderly people over a 9 year period showed that the use of the antioxidant vitamin E reduced the risk of death from all causes by 34%.  This effect was strongest for coronary artery disease, where vitamin E reduced death from heart attack by 63%. [American Journal of Clinical Nutrition, Aug. 1996]

Dosage: 750 to 1,500mg bid.  Important in fatty acid metabolism, depleted in cardiac muscle during acute infarctions.

Proline is involved in the structural repair of damaged collagen in arteriosclerotic blood vessels (hardened arteries).

Hawthorn is particularly recommended.  Proanthocyanadins stabilize collagen to prevent cholesterol deposits on arterial walls, prevent free radical damage, reduce peripheral vascular resistance, angina, cholesterol, and increase coronary and myocardial perfusion; hawthorn has a historic use in congestive heart failure; dosage 3 to 5gm as either dried herb, solid extract, or liquid extract.

Ginkgo (250mg tid) is also recommended.  Concentrated extracts may be required to achieve the recommended doses.  In addition, a tincture (30 to 60 drops tid) or tea (1 cup tid) of one to four of the suggested herbs, taken before meals, may be helpful.

A mechanism by which atherosclerotic plaque accumulates on the walls of arteries is the oxidation of LDL cholesterol.  Garlic has been shown in repeated studies to protect against LDL cholesterol oxidation and oxidation in the linings of the arteries themselves.  Garlic, ginger and onions all have a beneficial effect on platelet aggregation which reduces the tendency to form clots too easily, thus preventing the blockage of narrowed arteries.

A Seventh Day Adventist study that was reported at the 2002 International Congress on Vegetarian Nutrition found those that ate a serving of nuts 5 times per week had half the cardiac mortality.

A low-fat, low-cholesterol diet is recommended, as is an increase fiber (especially water-soluble fibers), fruits, vegetables, and vegetarian sources of protein.

A diet high in fiber helps prevent coronary heart disease.  Eating fruits high in the soluble fiber pectin has also been linked with reduced cholesterol levels, which protects against atherosclerosis.

Dosage: 150 to 250mg qid away from meals.  Inhibits platelet aggregation and breaks down plaque.

Regular aerobic exercise lowers fibrinogen levels – a risk factor for atherosclerosis of equal or greater predictive value than cholesterol.  Additionally, exercise improves the production of nitric oxide within the blood vessel wall, which should limit the progression of atherosclerosis.  Exercise improves the fitness of the heart as well as circulation.

Even damage from a history of heavy smoking can be reversed by quitting.  The longer the period of time that passes after quitting, the greater the return toward normal vascular health.

Magnesium is helpful in preventing blood vessel calcification (and thereby atherosclerosis).  A daily dose of 50mg of vitamin B6 and 200-300mg of magnesium is often given.

Considered to be from 200 to 500 times more potent an antioxidant than vitamin E, selenium and vitamin E are synergistic as antioxidants and inhibit or prevent the damage to tissues by free radicals which have been cited as causal factors in heart disease, atherosclerosis, arthritis and aging.  Dosage: 200mcg per day.

Chromium is often deficient in those with atherosclerosis; supplementation may result in plaque regression.  Chromium is used to help reduce atherosclerosis, especially in those who show low chromium levels.  Cultures with higher tissue levels of chromium also appear to have lower incidences of atherosclerosis and heart disease.  Dosage: 200mcg/day.

Mind/body techniques, such as yoga, meditation, relaxation, and biofeedback show promise in increasing cardiovascular health.

Cardiovascular risk factors that most highly predicted carotid artery wall thickness scores were holding anger in, being self-aware and having hostile attitudes.

Recycles vitamins E and C when they've been used.  Dosage: 50mg bid.

Dosage: 1,000mg tid.

Dosage: 400 IU per day.

For improved homocysteine metabolism, folic acid (800mcg per day), B6 (50mg per day), B12 (400mg per day), betaine (200 to 1,000mg per day) are recommended.

Lycopene has been used in connection with the prevention (only) of Atherosclerosis.