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Cardiovascular Support

Atherosclerosis is the silent killer responsible for coronary heart disease, cerebrovascular disease (stroke), and heart attack. In New Zealand alone over 35% of all people who die each year will have died of an illness due to atherosclerosis. In New Zealand amongst men, heart disease is the most common cause of death, with stroke being the fourth most common cause. In New Zealand women heart disease and stroke are the second and third most common causes of death respectively.

Atherosclerosis is a degenerative condition of the arteries characterised by an accumulation of lipids (mainly cholesterol, usually complex proteins and cholesterol esters) within the artery, which is known as an atherosclerotic plaque. The atherosclerotic plaque represents the end point of a complex, insidious process. Although any artery may be effected, the aorta, coronary, and cerebral vascular systems are most frequently involved.

Atherosclerosis begins at a very early age, even 1 year old infants show lesions in the aorta, which progresses to coronary artery abnormalities by the age of 10. This plaque will develop slowly and quietly over a period of years. Atherosclerosis is not usually diagnosed until the lesions suddenly precipitate a serious and often lethal, clinical condition. As the plaque increases in size, it begins to narrow the lumen of the artery, progressively reducing the blood flow, leading insufficient blood flow and the formulation at blood clots.

It is believed that atherosclerosis begins as damage to the lining of the artery. This is due to a number of factors; immune, physical, mechanical, viral, chemical, and drug factors have all been shown to damage the lining of the artery. Once the lining has been damaged it becomes more permeable to blood plasma constituents, especially lipoproteins (fat carrying proteins). This leads to a breakdown in the integrity of connective tissue in the artery and causes an increased affinity for cholesterol, the beginning of a plague. A fibrous gap consisting of collagen and other fibrous proteins develops over the plague, fats and cholesterol continue to accumulate. The plague continues to grow until it blocks the artery. Blockage is usually around 90% before the symptoms of arteriosclerosis are apparent.

Cholesterol: Foremost in the prevention of atherosclerosis is the reduction of serum cholesterol. Epidemiological evidence overwhelmingly associates hyperlipidemia with heart disease. In men and women 33 - 44 yr, those with serum cholesterol levels of over 256mg/dl have a 5x greater risk of developing coronary artery disease than those whose levels are below 250mg/dl.

Cholesterol levels are easily controlled by removing saturated fats form the diet, such as meat fats, and increasing essential mono-unsaturated and poly-unsaturated oils. Research has demonstrated that the ingestion of Omega-3 fish oils, particularly those high in Eicosapentaenoic Acid (EPA) and Decosahexaenoic Acid (DHA) is associated with a lower incidence of cardiovascular disorders, more favourable plasma lipid and lipoprotein levels, and reduced platelet aggregation.

Epidemiologically it has been demonstrated that Omega-3 fish oil consumption is inversely correlated with mortality from heart disease, while meat consumption is positively correlated.

 

 

Homocysteine: A new possibility for the cause of atherosclerosis has recently become apparent. This is a simple amino acid derivative of the essential amino acid, methionine, called homocysteine. Homocysteine is formed as a part of the natural process of protein break down, and is normally used by the body to: help manufacture proteins; produce the amino acids cysteine, taurine and glutathione; and carry out cellular metabolism. It now appears that a high level of homocysteine in the body can be a risk factor in the development of atherosclerosis.

Too much homocysteine appears to cause vascular walls to breakdown, exacerbating the development of atherosclerosis. Studies have also shown that high levels of homocysteine encourage blood platelets to clump together promoting clothing. This clotting ability combined with the increase in atherosclerosis leads to an increased likely hood of heart attacks or stroke.

As yet there is no explanations as to why some people over produce homocysteine, but the evidence seems to point to a shortage of vitamin B6, vitamin B12, and folic acid. All of which convert homocysteine into a form the body can easily use. The answer for people concerned about their cardiac health would seem to be to keep their vitamin intake high.

B12 and Folic Acid: Homocysteine can be recycled back to methionine through two chemical pathways the first of which involves folic acid. Folic acid donates a methyl group to homocysteine which converts it to methionine. Vitamin B12 is required as a co-factor of this reaction, ensuring that it progresses smoothly.

Betaine HCl: The second chemical pathway which recycles homocysteine to methionine involves betaine. This reaction, like the reaction above, involves the donation of a methyl group to the homocysteine molecule converting it to methionine. This reaction converts betain to dimethylglycine.

Vitamin B6: The formation of homocysteine is just one of many steps in the trans-sulphuration pathway. It is usually converted to cystathione as a normal part of the pathway, with this reaction requiring Vitamin B6. The progress of this reaction is based on the activity of the enzyme cystathione synthase, which is wholey dependant on the availability of vitamin B6. If deficiencies in vitamin B6 exist then the levels of vitamin B6 in plasma will increase.

Vitamin C: Strong clinical evidence suggests that a chronic latent Vitamin C deficiency can lead to hypercholesterolemia and the accumulation of cholesterol in certain tissues. Vitamin C helps prevent atherosclerosis directly through its inhibition of lipoprotein lipase, which promotes the catabolism of triglycerides, and through its regulation of arterial wall integrity via its essential role in collagen formation.

Vitamin E: Vitamin E is the premier lipid phase antioxidant. A deficiency results in an increased level of free radicals, particularly lipid peroxides, which can significantly lower levels of the antioxidant enzymes Superoxide Dismutase (SOD), GSH peroxidase, and catalase. This results in increased free radical damage, particularly of the linings of the arteries. Supplemental of Vitamin E has been shown to act as a potent free radical scavenger, inhibit platelet aggregation, and elevate HDL levels.

Magnesium: Epidemiological studies have shown that there is an inverse relationship between total body magnesium and atherosclerosis.

Magnesium has been referred to as "natures’ calcium channel blocker" because of its ability to block the entry of calcium into vascular smooth muscle cells and heart muscle cells. As a result, magnesium supplementation can help reduce vascular resistance, lower blood pressure, and lead to more efficient heart function. Population studies correlate a high magnesium intake with lower blood pressure. When tested in clinical trials the results have been mixed, but there is a general trend for a general decrease in blood pressure proportional to the amount of magnesium dosed.

Magnesium is beneficial in myocardial infarction as it is believed that magnesium is able to improve energy production in the heart.

Selenium: Low selenium levels in the blood are associated with an increased risk of heart disease. Restricted selenium intake reduces the functional activity of the antioxidant enzyme glutathione free radical damage to the lining of the arteries. These effects are aggregated by a vitamin E deficiency.

Bromelain: Bromelain is made up of a collection of small proteolytic (protein breaking) enzymes derived from the pineapple plant. Bromelain has been shown to inhibit platelet aggregation in vitro and in vivo, reduce blood pressure, and help in the breakdown of atherosclerotic plaques. These effects are based on bromelains ability to degrade protein.

Garlic: Garlic has been used by a large number of people throughout the world as a medical agent for a wide variety of illnesses. Although most recent research has been focused on its hypolipidemic effects, garlic has been shown to posses hypotensive qualities. In humans garlic has been shown by Collins et al (1990) to decrease systolic pressure by about 20-30 mmHg and diastolic pressure by about 10-20 mmHg.

In 1993 the American Journal of Medicine reported a study by Jain et al in which 42 healthy adults took either 300mg of standardised garlic powder in tablet form three times a day, or a placebo. After 12 weeks there was a significantly greater reduction in serum total cholesterol and LDL-cholesterol in those taking the garlic than in those taking the placebo A review covering experiments using fresh garlic by Kleijen et al (1989) found that garlic causes an increase in fibrinolytic activity (the breakdown of blood clots), inhibition of platelet aggregation and a lowering of cholesterol levels.

 

Hawthorne (Crataegus oxyacantha): Hawthorne, or mayflower as it is otherwise known, has been used historically as a heart tonic and is now used in Europe in the treatment of heart disease. The seventeenth-century English herbalist Nicholas Culpeper praised hawthorn as "a singular remedy for the stone [kidney stones], and no less effectual for dropsy [congestive heart failure]". American pioneers also used the plant for heart problems. The 19 century Eclectics prescribed it for the severe chest pain known as angina, and for congestive heart failure.

In Germany, where herbal medicine is more mainstream, three dozen hawthorn-based heart medicines are available.

Science appears to support what herbalists have long known, hawthorn is a heart stimulant. Hawthorne may help the heart in several ways:

    • It may open (dilate) the coronary arteries.
    • It may increase the hearts pumping force.
    • It may eliminate some types of heart-rhythm disturbances.
    • It may help limit the amount of cholesterol deposited on artery walls.

The leaves, berries and blossoms of hawthorn contain many biologically active flavonoid compounds. Hawthorne berries and flowers are a particularly good source of anthocyanidins and proanthocyanidins. Included in their effects are an ability to increase intracellular vitamin C levels and decrease capillary fragility and permeability. The beneficial and pharmacological effects of hawthorn extracts in the treatment of high blood pressure appear to be a result of dilating the larger blood vessels.

Co-enzyme Q10: Coenzyme Q10, or ubiquinone, is a vitamin-like substance which is made by our bodies which is found in the mitochondria of cells. The highest proportion of mitochondria are found in organs that do the most work, notably the liver, muscle tissue and the heart. Mitochondria are the intracellular structures that manufacture ATP (Adenosine Triphosphate), the basic energy molecule of cells. Through a series of chemical reactions food is broken down to its component parts and these are combusted with oxygen to make a unit of ATP.

The heart has high energy requirements and also high concentrations of coenzyme Q10. Because natural stores drop with age, focus has turned to coenzyme Q10 as a cardiac nutrient. Levels of coenzyme Q10 have been found to be significantly lower in people with heart problems. It has been shown to enhance the pumping action and electrical functioning of the heart as well as lower blood pressure. This all helps to improve heart function.

Coenzyme Q10 may inhibit the synthesis of cholesterol since it has some metabolic processes in common with cholesterol. It acts as an antioxidant which scavenges harmful free radicals, supports the function of vitamin E in the body and also helps recycle vitamin E. The antioxidant function of coenzyme Q10 may enhance its role in the prevention of heart disease and heart problems.

Dosage:

Take two to four capsules, or as professionally prescribed. For best results, take with magnesium absorb and L-carnitine

Caution:

Not to be taken by pregnant or lactating women.

Supplement Facts

At the time of manufacture, each capsule contained not less than:

Ingredient

mg/Cap

Hawthorne Extract 4:1

600

Coenzyme Q10

15

Magnesium Citrate 30%

21

Bromelain 2000 GDU/g

50

Garlic Extract 100:1

1500

Omega-3 25%

15

Pyridoxine (Vitamin B6)

12.5

Cyanocobalamin (B12) 1 %

0.0125

Folic Acid

0.05

Betaine HCl

12.5

Ascorbic Acid (Vitamin C)

20

D--Tocopherol (Vitamin E)

10

Selenium Chelate 0.5%

0.0375

Zinc Methionine 20%

3.75

Potassium Chelate 20%

3.75

* some herbal extracts used

References

Collins R., Peto R., MacMahon S. et al. 1990 Blood pressure, stroke and coronary heart disease, Part 2. Short term reduction in blood pressure. Overview of randomised drug trials in their epidemiological context. Lancet. 335: 827-838.

Jain A.K., Vorgas R., Gotzkowsky R.N., McMahon F.G. 1993 Can garlic reduce levels of serum lipids? A controlled clinical study. The American Journal of Medicine (94): 632-635.

Kleijen J., Knipschild P., Ter Reit G. 1989 Garlic, onions and cardiovascular risk factors. A review of the evidence from human experiments with emphasis on commercially available preparations. Br. J. Clin. Pharmac. 28: 535-544.

Mortensen S. A., Vadhanavikit S., Muratsu K., Folkers K. 1990 Coenzyme Q10: Clinical benefits with biochemical correlates suggesting a scientific breakthrough in the management of chronic heart failure. Int J Tiss Reac XII(3): 155-162.

Bertelli A., Ronca G. 1990 Carnitine and coenzyme Q10: Biochemical properties and functions, synergism and complementary action. Int J Tiss Reac XII(3): 183-186.

Greenberg S., Frishman W. H. 1990 Coenzyme Q10: A new drug for cardiovascular disease. J Clin Pharmacol 30: 596-608.

Castleman, M. (1991) The Healing Herbs. Melborne: Schwartz books.

Murray, M., Pizzorno, J. (1990) Encyclopaedia of Natural Medicine. London: Macdonald and Co. Ltd.

Pizzorno, J., Murray, M. (1993) A textbook of Natural Medicine. Seatle, USA: Bastyr University Publications.

Murray, M. (1996) Encyclopedia of Nutritional Supplements. Rocklin, USA: Prima Publishing.

Public Health Commission (1993) Our Health Our Future. Wellington, New Zealand: Public Health Commission.

Perry, I. (1996) Serum total homocysteine concentration and risk of stroke. Lancet 30;348(9040):1526

 

 

 

 

 

 

 

 

 

 

 

 

 

 
 
 
 
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