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http://www.newswithviews.com:80/Howenstine/james67.htm

PART 1 of 2

 

 

 

By Dr. James Howenstine, MD.

July 24, 2008

 

NewsWithViews.com

 

Vitamin K2 Removes Calcium From Arteries And Deposits It In Bone

 

Detecting calcium deposits in arteries by computer tomography scanning studies

has become a valuable clue that an individual has arteriosclerotic heart disease

and has significant risk for heart attack and sudden death. Detected calcium

arterial deposits thus permit life style changes to be instituted before sudden

death or acute myocardial infarction has occurred. This increased risk of

calcium deposition into arteries has recently been confirmed to bring increased

risk of heart attack and heart disease deaths to blacks, Hispanics and

Chinese[1] even though their risks are less than Caucasians.

 

Western cultures (Northern Europe, Canada, USA,) eat a high protein, high dairy,

high phosphorus acidifying diet. This type food causes large amounts of calcium

to be wasted in the urine as it is removed from bone tissue to try to preserve

an alkaline cellular environment in the face of a very acidic dietary protein

intake. To make matters even worse the ratio of calcium to magnesium in milk is

9 to 1 which exaggerates the lack of magnesium found in food grown on magnesium

depleted U.S. soil. Low magnesium stores in bone cells prevents magnesium from

being of any value in attempts to preserve an alkaline body pH. Naturally the

Western diet leads to profound loss of calcium and magnesium from bone thus

ensuring osteoporosis and fractured bones in the elderly. The nation of Thailand

which eats almost no dairy products and obtains calcium primarily from

vegetables has much less osteoporosis than western nations on their high protein

high dairy product diets.

 

Calcification in cellular tissues is a sign of tissue damage, cellular aging and

impending cell death. When cells are unable to regulate calcium and keep the

calcium content of cells down cellular function degenerates. Calcified arteries,

calcium in soft tissues and high levels of calcium within cells are all signs of

aging. At age 80 the average calcium content in the aorta is 140 times

greater[2] than the levels of aortic calcification noted at age 40. This may

relate to a long period of unrecognized Vitamin K2 deficiency.

 

Vitamin K1 is found in plants and Vitamin K2 is found in animals and bacteria

(healthy colon bacteria, Japanese natto, low fat Dutch gouda and edam cheese).

Bacteria in the colon are able to produce and store about one month of Vitamin

K. Antibiotics kill many of these good intestinal bacteria thus impairing

production of Vitamin K. The non-steroidal anti-inflammatory drugs have similar

adverse effects on these valuable bacteria. Vitamin K absorption is improved by

dietary fat which stimulates bile secretion.

 

Studies have shown that subclinical Vitamin K deficiency,[3] [4] is present in

most healthy adults. The first symptoms of this deficiency can be heart attack

or a fractured osteoporotic bone. In the Framingham study subjects in the

highest quartile for Vitamin K intake had a significantly lower risk[5] of hip

fracture.

 

In 1984 scientists reported that patients with osteoporotic fractures had

circulating Vitamin K1 levels that were 70%[6] lower than age and sex matched

controls. These findings were confirmed and it was noted that low levels of

Vitamin K were associated with loss of bone mineral density creating an

independent risk factor for bone fracture. Further studies have disclosed that

Vitamin K1 was less effective than Vitamin K2 in preventing bone loss.

 

The absorption of synthetic Vitamin K1 has recently been compared to the

absorption of Vitamin K2(menaquinone-7) in healthy subjects. Vitamin K1 has been

widely used in food supplements. Recently natural Vitamin K2 has become

available for use in supplements. Both Vitamin K1 and Vitamin K2 were well

absorbed with peak blood levels reached at 4 hours. Unlike Vitamin K1, Vitamin

K2 was found to have a very long half life which results in stable higher blood

levels. During prolonged intake the long half life permits accumulation Of K2 to

levels 7-8 fold higher than that seen after one dose. Vitamin K2(MK-7) is 6

times more potent than Vitamin K1.

 

Use Of Vitamin K2(Menaquinone-7) To Prevent Calcium Plaques From Appearing In

Arteries

 

The commonly used anticoagulant drug coumadin interferes with the metabolism and

function of Vitamin K by inhibiting the enzymes needed to produce Vitamin K This

drug can produce excessive bleeding and does produce progressive widespread

calcification of arteries and the aorta.

 

A clinical study from Rotterdam, Holland revealed a correlation between long

term adequate Vitamin K2 intake and a lower incidence of calcification of the

wall of the aorta. Arteries with no plaques have a 20 to 50 fold increase in

Vitamin K2 concentration when compared to arteries with arterial plaques. The

high K2(menaquinone-7) content arteries were noted to be more flexible[7] and

elastic than arteries lacking K2.

 

Lack of Vitamin K2 causes calcium to fail to be deposited in bones where it

belongs and to be deposited instead in arteries, aorta, soft tissues including

muscle, breast, kidneys and in heel spurs.

 

A protein called osteocalcin transports calcium to bone. Vitamin

K2(menaquinone-7) is used to solidify this calcium into the bone matrix. When

Vitamin K2 is lacking the calcium remains in the blood and ends up getting

deposited in the walls of arteries and other sites which is very undesirable.

Thus Vitamin K2 becomes a critical nutrient for both bone and arteries. The

primary therapy for osteoporosis in Japan has become Vitamin K2(Synergy K).

 

Dr. Leon Schurgers and Dr. Cees Vermeer of Maastricht University in Holland

studied 4800 elderly Dutch men and women to ascertain whether Vitamin K2 could

help prevent artery calcium deposits. They learned that persons with the highest

dietary intake of K2 (primarily originating in low fat Dutch cheeses Gouda and

Edam) had the least evidence of calcification of the aorta[8] when compared to

persons with low Vitamin K2 intakes. The higher the intake of these cheeses the

lower the mortality from cardiovascular disease.

 

The fermented soy Japanese food natto contains Vitamin K2 in large amounts but

Americans are likely to find it's taste and smell objectionable unless it is

covered by sauces. All of the Vitamin K2 produced in making the enzyme

nattokinase has now become available to be sold for use in food supplements.

 

The drug coumadin is widely used by conventional medicine in cardiovascular

disease to prevent clotting. Numerous natural health experts have been concerned

for years that coumadin was not effective in preventing vascular deaths but also

has problems with occasional serious internal bleeding episodes.

German researchers[9] found out in 2005 that long term use of coumadin produced

increased calcium in the aortic valve and coronary arteries when compared to

patients not taking coumadin. Dr. Gary Gordon states that " every patient on

coumadin is increasing the calcium content of all vascular tissues. The

calcium[10] content of arteries is now proven to be more dangerous than

diabetes, elevated cholesterol or hypertension, we must now try to educate

patients. " Patients taking coumadin can be easily moved to safer anticoagulant

therapy.

 

This information proves that Vitamin K2 is a critical nutrient for patients with

arteriosclerosis as it has the potential to prevent and remove calcium from

arteriosclerotic plaques thus making plaques easier to dissolve and less

dangerous..

 

Vitamin K2 is now available as Synergy K. One capsule of Synergy K contains 45

mcg of Vitamin K2(Menaquinone-7) and 1 mg of (Menaquinone-4 less well absorbed

than K2). Natural Health Team 1-800-416-2806 can supply Synergy K. The dose

should be one capsule daily(45 mcg.).

 

Arteriosclerosis Caused by Elevated Homocysteine, and its Correction

 

Methionine from red meat, milk, and milk products is converted in the body into

homocysteine. When the body's stores of B6 (pyridoxine), folic acid, and B12

fail to bring this homocysteine down to normal values, there is a three times

greater risk of heart attack than in males with normal homocysteine values.

 

Dr. Kilmer McCully gets credit for discovering the critical role that

homocysteine plays in the genesis of arteriosclerosis. Homocysteine stops the

production of the valuable vasodilating nitric acid, causes blood to thicken,

and facilitates the oxidation of LDL cholesterol, thus setting the stage for an

atherosclerotic plaque to form. As more patients are studied, it has become

evident that elevated levels of homocysteine are a common cause for

arteriosclerosis (at least 40% of patients).

 

If you have artery problems, measuring homocysteine in the blood will frequently

provide clear evidence that homocysteine is causing the problem, not

cholesterol. The homocysteine blood test should become part of annual laboratory

tests and is particularly important for smokers, diabetics, hypertensives,

patients with familial hypercholesterolemia and persons who have had stokes,

heart attacks, angina and claudication( arteriosclerosis of aorta and leg

arteries).

 

A Norwegian[11] study discovered that in 587 patients with coronary heart

disease, the risk of death within four years was proportional to total plasma

homocysteine level. The risk rose from 3.8% with homocysteine below nine

micromols per liter to 24.7% in patients with homocysteine levels above 15

micromols per liter.

 

The only way to be certain that you are getting the proper dosage of folic acid,

vitamin B12, vitamin B6, and trimethylglycine to treat homocysteine excess is to

have regular blood homocysteine HC tests. Each 3-unit increase in HC causes a

35% increase[12] in the risk of heart attack.

 

Trimethylglycine (TMG) - also called Glycine Betaine - is the most effective[13]

agent to lower homocysteine levels. The usual dose is 500 mg three times daily.

If HC levels have not fallen adequately, up to 9000 mg of TMG may be needed

daily.

 

Folic acid (800 mcg with each meal) and 1000 mcg of B12 daily are also vital.

 

B6 (pyridoxine) reduces HC by a different method than folic acid. The dose of B6

should be 100 to 200 mg daily.

 

In a patient with previous bypass surgery, angina reappeared along with new

areas of blockage of heart arteries. This man was taking 15,000 mcg of folic

acid daily. His blood homocysteine (HC) level was very high risk at 18. On six

grams daily of trimethylglycine, his HC fell to four in one month.

 

Trimethylglycine functions in treating elevated HC levels by donating methyl

groups, which convert HC to the harmless amino acid methionine. Trimethylglycine

(Glycine Betaine) can be purchased in health food stores.

 

A new organic form of Vitamin B Complex (Supreme B) is producing remarkable

improvement in cardiac patients as well as healing a wide variety of neurologic

disorders by promoting healing and growth of new nerve dells. Supreme B can be

obtained from Lifeone Sales, 1-407-349-2241 sales or from

www.mynaturalhealthteam.com Ph 1-800-416-2806.

 

Vitamin C and Lysine

 

Research by Dr. Linus Pauling and Dr. Mattias Rath demonstrated that 2 grams of

Vitamin C and 2 grams of the amino acid Lysine each taken three times daily was

very effective in healing arteriosclerotic arteries.

 

Traditionally Low Density Lipoprotein was blamed for causing the atherosclerotic

plaque. However, the actual culprit is a very sticky substance known as

lipoprotein (a). Lysine was added to Vitamin C therapy because it has a surface

like Teflon which tends to repel the sticky lipoprotein(a). The Lysine and

another aminoacid proline surround particles of lipoprotein (a). This seals off

the lipoprotein (a) so that it can not attach more lipoprotein (a) preventing

the plaque from becoming larger. Additionally lipoprotein (a) previously

deposited in the artery wall begin to be released into the blood stream. These

lipoprotein deposits are transported to the liver where they are burned up. Thus

the size of the plaque starts to decrease. This is a natural process which

proceeds uneventfully until the plaque is gone.

 

Lipoprotein(a) is a 10 times more dangerous risk factor than Low Density

Lipoprotein or cholesterol. Within 6 to 8 weeks of starting lysine and vitamin C

many patients had experienced loss of anginal pain, disappearance of

hypertension and the ability to pass an exercise treadmill test.

 

These investigators proposed that arteriosclerosis was actually caused by

deficiency of Vitamin C which the body needs to create the structural substances

collagen and elastin which are used to form the framework of connective tissue

and elastic tissue. Patients lacking Vitamin C use the sticky substance

lipoprotein (a) to try to solidify the weak spots in arteries which lack

collagen fibers. Lipoprotein (a) sticks to irregular areas on the lining of the

arteries and proceeds to collect platelets, calcium, lipoproteins (LDL),

lipoprotein (a) and fibrin from the arterial blood flow. Over time scar tissue

appears and smooth muscle fibers may appear. This build up of the plaque reduces

the speed of blood flow and interferes with proper oxygenation of tissues.

Anginal pain, transient ischemic attacks in the brain circulation as tiny and

large fragments of plaque break off and get carried to more distal sites in the

brain arteries, .and actual death of tissue(gangrene in extremities, stroke,

heart attack) from extreme lack of oxygenation can result.

 

Pathologists have long observed that arterial plaques are commonly seen where

the forceful arterial stream strikes an arterial wall. This location is

frequently at the site where the coronary arteries branch off the aorta. The

steady strong force of the arterial stream causes the weak artery wall lacking

Vitamin C to seek the reinforcement of additional lipoprotein (a) making a

buildup of large plaques at this site very common. If cholesterol was a

dangerous toxic substance the occurrence of arterial plaques would be completely

random rather than appearing at sites where the arterial wall is being steadily

traumatized. This information creates a strong argument that cholesterol is not

a primary cause for vascular disease. Additionally we know that more than 50% of

patients having an acute myocardial infraction have perfectly normal cholesterol

values.

 

Dr. Matthias Rath[14] and colleagues did research which revealed that

lipoptotein (a) is an LDL particle surrounded by a very adhesive protein. Their

study disclosed that the plaque is largely composed of lipoprotein (a) rather

than LDL molecules. The size of the plaque paralleled the amount of lipoprotein

(a) particles deposited in the arterial plaque.

 

Lipoprotein (a) blood levels vary greatly from person to person. The levels are

determined by heredity and are not lowered by special diets. Lipoprotein (a)

values can be lowered by 36% in patients taking 2 to 4 grams of Vitamin B3

(nicotinic acid). Vitamin C alone or combined with nicotinic acid may have a

lowering effect on the production of lipoproteins .resulting in lower

lipoprotein values. When these therapies are combined with lysine and proline

the cardiovascular risk of lipoprotein (a) can be reduced.

 

Animals that easily produce Vitamin C have low levels of lipoprotein (a). Thus

humans, guinea pigs and a few primates that fail to produce Vitamin C are able

to inadequately repair arteries by virtue of having access to lipoprotein (a).

 

Very few Americans are consuming more than a gram of Vitamin C daily. Humans,

primates, and guinea pigs lack the L-gulonolactone oxidase GAL enzyme. All other

animals are able to manufacture ascorbate from glucose and thus become able to

handle stress far better than humans who invariably fail hopelessly in producing

the 30 to 100 grams of ascorbate daily that may be necessary to combat a

stressful event.

 

© 2008 Dr. James Howenstine -

 

 

 

 

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