Atherosclerosis - Treatment - Diet and Dietary Supplements

Diet and Dietary Supplements

Niacin (vitamin B₃), in pharmacologic doses, (generally 1,000 to 3,000 mg/day, but starting with much lower doses increased over several weeks, to avoid side-effects) tends to improve (a) HDL levels, size and function, (b) shift LDL particle distribution to larger particle size and (c) lower lipoprotein(a), an atherosclerosis promoting genetic variant of LDL. Additionally, individual responses to daily niacin, while mostly evident after a month at effective doses, tends to continue to slowly improve further over time. (However, careful patient understanding of how to achieve this without nuisance symptoms is needed, though not often achieved.) Research work on increasing HDL particle concentration and function, beyond the usual niacin effect/response, even more important, is slowly advancing. Niacin is supplied in many OTC and prescription formulations; non-prescription formulations recommend much lower doses as they are sold as nutritional supplements, not regulated medications.

Dietary changes to achieve benefit have been more controversial, generally far less effective and less widely adhered to with success. One key reason for this is that most cholesterol, typically 80-90%, within the body is created and controlled by internal production by all cells in the body (true of all animals), with typically slightly greater relative production by hepatic/liver cells. (Cell structure relies on fat membranes to separate and organize intracellular water, proteins and nucleic acids and cholesterol is one of the components of all animal cell membranes.)

While the absolute production quantities vary with the individual, group averages for total human body content of cholesterol within the U.S. population commonly run about 35,000 mg (assuming lean build; varies with body weight and build) and about 1,000 mg/day ongoing production. Dietary intake plays a smaller role, 200–300 mg/day being common values; for pure vegetarians, essentially 0 mg/day, but this typically does not change the situation very much because internal production increases to largely compensate for the reduced intake. For many, especially those with greater than optimal body mass and increased glucose levels, reducing carbohydrate (especially simple forms) intake, not fats or cholesterol, is often more effective for improving lipoprotein expression patterns, weight and blood glucose values. For this reason, medical authorities much less frequently promote the low dietary fat concepts than was commonly the case prior to about year 2005. However, evidence has increased that processed, particularly industrial non-enzymatic hydrogenation produced trans fats, as opposed to the natural cis-configured fats, which living cells primarily produce, is a significant health hazard.

Dietary supplements of Omega-3 oils, especially those from the muscle of some deep salt water living fish species, also have clinical evidence of significant protective effects as confirmed by 6 double blind placebo controlled human clinical trials.

Less robust evidence shows that homocysteine and uric acid levels, including within the normal range, promote atherosclerosis and that lowering these levels is helpful.

In animals Vitamin C deficiency has been confirmed as an important role in development of hypercholesterolemia and atherosclerosis, but due to ethical reasons placebo-controlled human studies are impossible to do. Vitamin C acts as an antioxidant in vessels and inhibits inflammatory process. It has therapeutic properties on high blood pressure and its fluctuation, and arterial stiffness in diabetes. Vitamin C is also a natural regulator of cholesterol and higher doses (over 150 mg/kg daily) may confer significant protection against atherosclerosis even in the situation of elevated cholesterol levels.

The scale of vitamin C benefits on cardiovascular system led several authors to theorize that vitamin C deficiency is the primary cause of cardiovascular diseases. The theory was unified by twice Nobel prize winner Linus Pauling, and Matthias Rath (Rath's promotion of vitamins instead of effective medicines for treatment of serious diseases has been very strongly criticised by many reputable authorities, as discussed in detail elsewhere). They point out that vitamin C is produced by almost all animals, with few exceptions including mankind and the great apes. This is due to a genetic deficiency that arose with the common ancestor of human and apes. To survive humans and apes must eat sufficient vitamin C. Without vitamin C humans develop scurvy. Vitamin C is an essential element in insuring that the vascular system is strong and flexible. Pauling and Rath suggest that a deficiency causes weakness in the arterial system and the body compensates by trying to stiffen up the artery walls using other common blood elements. This causes the effect known as atherosclerosis. They suggest that clinical manifestations of cardiovascular diseases are merely overshoot of body defense mechanisms that are involved in stabilisation of vascular wall after it is weakened by the vitamin C deficiency and the subsequent collagen degradation. They discuss several metabolic and genetic predispositions (our inability to produce vitamin C at all being the main one) and their pathomechanism.

The Unified Theory of Human Cardiovascular Disease suggests that atherosclerosis may be reversed and cured, but there has been no testing or trial of Pauling's vitamin C theory.

Trials on Vitamin E have been made, and have generally not found a beneficial effect. It has been suggested that there may be a beneficial effect for some patients at high risk for atherosclerosis. A review of trials suggested that the lack of evidence for a beneficial effect may have been due to various specified shortcomings in the trial methodologies, such as testing vitamin E without concurrent use of vitamin C.

Menaquinone (Vitamin K₂), but not phylloquinone (Vitamin K₁), intake is associated with reduced risk of CHD mortality, all-cause mortality and severe aortic calcification.

Excess iron may be involved in the development of atherosclerosis, but one study found reducing body iron stores in patients with symptomatic peripheral artery disease through phlebotomy did not significantly decrease all-cause mortality or death plus nonfatal myocardial infarction and stroke. Further studies may be warranted.

Dietary iodine deficiency and hypothyroidism which are cause of elevated serum cholesterol and of lipid peroxidation, may be involved in the development of atherosclerosis, in fact radioiodide (131-I) is detectable in radioautographies of elastic arterial walls until 14 days after subcutaneous injection, suggesting a specific (probably antioxidant ) role in arterial walls. Kocher observed that atherosclerosis, thought to be caused by ROS, frequently appeared following thyroidectomies, suggesting that hypothyroidism is causally associated with atherosclerosis. Iodides were used empirically in patients with arteriosclerosis and cardiovascular diseases by European physicians. Turner reported efficacy of iodine and desiccated thyroid in prevention of atherosclerosis in rabbits. The antioxidant action of dietary iodides has been described in prevention and in therapy of some human chronic diseases and also of atherosclerosis -

Changes in diet may help prevent the development of atherosclerosis. Researchers at the Agricultural Research Service have found that avenanthramides, chemical compounds found in oats, may help reduce the inflammation of the arterial wall, which contributes to the development of atherosclerosis. Avenanthramides have anti-inflammatory properties that are linked to activating proinflammatory cytokines. Cytokines are proteins that are released by the cell to protect and repair tissues. Researchers found that these compounds in oats have the ability to reduce inflammation and thereby help prevent atherosclerosis.