Vitamin A and Beta-Carotene-- lower fibrinogen levels and heart disease risks and increase insulin sensitivity
Dexter Morris, M.D. (University of North Carolina), says that phytochemicals keep your heart healthy. "The 60-80 age group has a much greater risk of heart disease than younger people do. If your diet is rich in fruits and vegetables, you can reduce risk," according to Morris. In a study begun in 1973, researchers kept track of 1883 men ages 35-59 who had high cholesterol levels. Over the next 20 years, the men who had the highest levels of carotenoids in their blood had 60% fewer heart attacks and deaths (Morris 2001).
Dr. J.E. Manson of the Women's Hospital in Boston reported that those taking 25,000 IU of beta-carotene daily had 22% fewer heart problems and strokes than those taking less than 10,000 IU daily (Friend 1991; Passwater undated). Dr. Monika Eichholzer (scientist at the University of Bern, Switzerland) reported similar findings after tracking 2974 people for 12 years. The relative risk of ischemic heart disease was increased (1.53%) among those lowest in plasma carotene concentrations (Eichholzer et al. 1992).
High vitamin A and beta-carotene serum levels have been reported to reduce fibrinogen levels in humans and animals (Green 1997). Animals fed a vitamin A-deficient diet have an impaired ability to break down fibrinogen, but when injected with vitamin A, they produce tissue plasminogen activators that break down fibrinogen, reducing the risk of clot formation.
Vitamin A is beneficial to individuals with Syndrome X and diabetes. A study involving 52 patients indicated that vitamin A enhanced insulin-mediated glucose disposal (Facchini et al. 1996a). Since beta-carotene must be converted in the body to vitamin A, an adaptation some individuals lack, diabetics may do better using vitamin A rather than beta-carotene.
It should be noted that the protection of beta-carotene is not absolute. If the individual is consuming greater amounts of alcohol, beta-carotene may actually increase the risk of intracerebral hemorrhage (Leppala et al. 2000). A blend of phytoextracts (alpha-carotene, beta-carotene, lutein, and lycopene) appears to offer more comprehensive cardiac protection than using beta-carotene alone.
For example, individuals participating in the Toulouse study who had higher blood levels of lutein also had a lower incidence of coronary artery disease (Howard et al. 1996). The Los Angeles Atherosclerosis study uncovered a relationship between thickenings in the carotid arteries (an indicator of systemic atherosclerosis) and blood levels of lutein (Dwyer et al. 2001). Participants with the highest blood levels of lutein showed virtually no artery wall thickening, while those with the lowest lutein levels showed increased arterial thickness. Lutein also reduces the oxidation of LDL cholesterol.
A current Finnish study evaluated 725 middle-aged men free of coronary heart disease and stroke at the study baseline. Men in the lowest quartile of serum levels of lycopene had a 3.3-fold risk of an acute coronary event or stroke compared with other trial participants with higher lycopene levels. In a second study, the same researchers assessed the association between plasma concentrations of lycopene and intima-media thickness (IMT) of the common carotid artery wall in 520 asymptomatic men and women. After adjusting for common cardiovascular risk factors, low plasma levels of lycopene were associated with an 18% increase in IMT in men as compared with men in whom plasma levels were higher than median. In women, the difference did not remain significant after the adjustments (Rissenen et al. 2002).
German researchers reported that plasma levels of alpha-carotene may represent a marker of atherosclerosis in humans. Measuring alpha-carotene levels (among other antioxidants) may be of clinical importance as a practical approach to assess atherogenesis and/or its risk (Kontush et al. 1996).
Some individuals are susceptible to vitamin A toxicity even when the dosage is low. This occurs because of a challenged liver and fewer detoxification mechanisms. Beta-carotene, on the other hand, is generally regarded as nontoxic. Appropriate dosages for most individuals are 5000 IU of beta-carotene and/or 10,000 IU of vitamin A daily.
Reader's guide to vitamin A food sources, enhancers, and agonists: The richest sources of vitamin A are foods of animal origin, i.e., liver, fish liver oil, milk and milk products, butter, and eggs. Yellow fruits and green and yellow vegetables will also help meet vitamin A requirements.
Enhancers to vitamin A absorption are vitamin C, calcium, magnesium, vitamin E, B complex, choline, and essential fatty acids. Vitamin A antagonists are laxatives and some cholesterol-lowering drugs (Questran). Coffee, alcohol, excess iron supplementation, sugar, tobacco, and mineral oil can also interfere with vitamin A absorption. Food sources of lutein are kale, Brussels sprouts, corn, collards, spinach, and egg yolks. Egg yolks have tiny amounts of lutein -- about 0.2 mg a yolk -- because chickens eat corn (Carper 2002). Lycopene is present in tomatoes and several other red fruits.
Vitamin C-- lessens risk of stroke and heart attack; strengthens blood vessels; reduces blood pressure, fibrinogen levels, Lp(a), inflammation, and C-reactive protein (CRP); promotes gingival healing; is a reliable antioxidant and diuretic; and is highly beneficial to smokers and those exposed to secondhand smoke
Linus Pauling, a Nobel Prize winner, showed that the body often forms atherosclerotic plaque to repair a wound inflicted upon an artery. When adequate amounts of vitamin C are available, an injured artery is repaired without involving atheromatous materials. In the absence of adequate levels of vitamin C, Lp(a), acting as a surrogate for vitamin C, must participate in the repair. Lp(a) does what it must, but the health of the artery is compromised as plaque is added to the vessel.
Kathie M. Dalessandri, M.S., M.D., was inspired by a report appearing in the Archives of Internal Medicine relating to the ability of vitamin C to lower Lp(a). Dr. Dalessandri, a general surgeon in Point Reyes Station, CA, was displeased with her own Lp(a) levels. She was well aware of the dangers associated with Lp(a), particularly when linked with other risk factors as a family history of heart disease. Dr. Dalessandri (53 years old at the time) was taking hormone replacement therapy and niacin, but the niacin became problematic and had to be discontinued. After reviewing the literature, she decided upon 3 grams a day of both ascorbic acid and L-lysine monohydrochloride as a natural regime against the elevated Lp(a). Dr. Dalessandri reports that her Lp(a) dropped 14 mg/dL, a reduction of 48% after 6 months. She was also pleased that she was able to take vitamin C and lysine without side effects (Dalessandri 2001).
Matthias Rath, M.D., in Eradicating Heart Disease, says that animals do not have heart attacks and strokes because their bodies manufacture vitamin C, a genetic adaptation humans lack. Most mammals produce impressive amounts of vitamin C, the human equivalency of 2000-13,000 mg daily. Under periods of stress the same animal's needs for vitamin C may skyrocket, but the body complies by producing prodigious amounts. Man cannot adapt to stress with the same efficiency as lower animals because of a lack of L-gulonolactone oxidase, an enzyme needed to produce vitamin C from glucose. Dr. Rath states that because of this genetic flaw and inadequate dietary vitamin C, cardiovascular disease can emerge as a form of early scurvy (Rath 1993).
An ascorbic acid deficit contributes to the development of vascular lesions (wounds or injuries) by altering collagen metabolism (Rath 1993). Vitamin C produces many collagen molecules, supporting a strong and elastic blood vessel wall. Over time, arterial collagen must be replenished. If vitamin C is not present in large enough quantities, collagen is not produced, and blood vessels become thin and weak.
Vitamin C levels are lower in patients who have had heart attacks, both fatal and nonfatal events. Randomly selected Finnish men (1605 individuals who were 42-60 years old) entered a study evidencing no signs of preexisting heart disease. Among men with a vitamin C deficiency, 13.2% had a heart attack compared to 3.8% who were not vitamin C deficient. After adjusting for other confounding factors, men who were deficient in vitamin C had 3.5 times more heart attacks than men who were not vitamin C deficient (Nyyssonen et al. 1997).
The most significant report emanated from UCLA, where it was announced that men who took 300-400 mg of vitamin C a day lived 6 years longer than those who received less than 50 mg daily. The study (which evaluated 11,348 participants over a 10-year period) showed that long-term, high vitamin C intake extended average lifespan and reduced mortality from cardiovascular disease 45% (Enstrom et al. 1992; Hansen 2000).
Researchers from the Boston University School of Medicine reported that vitamin C appears effective in lowering mild cases of hypertension. The patients lowered systolic and diastolic blood pressure by about 9% with a daily dose of 500 mg of ascorbic acid (Stauth 2001). The value of vitamin C as a hypotensive nutrient may come by way of its antioxidant activity, possibly by protecting the body's supply of NO, a vasodilator. Depriving test animals of antioxidants, such as vitamin C, glutathione, and vitamin E, resulted in oxidative stress and higher blood pressure.
The heart is one of the most vulnerable of all organs to free-radical oxidative stress. Vitamin C can respond to this risk by exerting its antioxidant properties, acting independently, or by prompting the production of other antioxidants. For example, 3 grams of vitamin C increased white blood cell glutathione levels fourfold and plasma glutathione levels eightfold (Jain et al. 1994; Murray 1996b).
Vitamin C is beneficial in reducing fibrinogen levels. In a report published in the journal Atherosclerosis, heart disease patients were given either 1000 or 2000 mg a day of vitamin C to assess its effect on the breakdown of fibrinogen. At 1000 mg a day, there was no significant change in fibrinolytic activity. At 2000 mg of vitamin C a day, fibrinolytic activity increased 62.5% (Bordia 1980).
Inflammation, a newer risk factor for heart disease, is reduced by vitamin C. Each winter (in most countries) there is a 15-30% increase in deaths from cardiovascular and respiratory disease. Researchers in the United Kingdom followed 96 men and women for 1 year to assess the impact of winter stress upon the heart and circulatory system. It appears some of the increase in winter cardiovascular mortality may be related not only to a rise in fibrinogen, but also to an increase in other inflammatory markers, such as C-reactive protein. This cycle may be spurred as winter infections increase and vitamin C intake decreases. The conclusion of the study was that vitamin C might be able to influence cardiovascular risk and the resulting thrombotic tendency by modulating the inflammatory response to infection (Woodhouse et al. 1997).
Vitamin C appears to lessen the negative effects of other risk factors, including stress, diseased gums, unhealthy diet, and smoking. Smoking severely depletes the body of vitamin C; vitamin C, on the other hand, destroys free radicals produced in smoke and protects against endothelial dysfunction. Secondhand smoke breaks down blood antioxidant defenses and accelerates lipid peroxidation, which leads to an accumulation of LDL cholesterol (Tribble et al. 1993). Vitamin C fights against the ravages of both firsthand and passive smoke.
A dosage suggestion is 6 grams daily in divided dosages. (A loose stool may result from higher doses of vitamin C. Should this occur simply reduce the dose to a level that is not problematic to the bowel.) Under periods of stress, a great deal more vitamin C can be taken without bowel derangement.
Reader's guide to vitamin C food sources, enhancers, and antagonists: Vegetables and fresh, uncooked fruits (especially citrus) are vitamin C-rich sources. Raw foods represent excellent choices.
All vitamins and minerals work synergistically to enhance vitamin C absorption, particularly the bioflavonoids. Alcohol, coffee, sulfa drugs, antibiotics, analgesics, antidepressants, anticoagulants, oral contraceptives, and steroids can drain vitamin C from the body. Smoking seriously depletes vitamin C levels.
Vitamin D-- reduces heart disease risk in women
It was reported at the 42nd annual conference on Cardiovascular Disease and Epidemiology Prevention (in Honolulu, HI, on April 23, 2002) that women who take vitamin D supplements lowered their risk of death from heart disease by one-third. The finding was an unexpected dividend extracted from an osteoporosis trial to determine the incidence of bone fracture in nearly 10,000 older women. From the trial participants, 4200 women reported taking vitamin D supplements at the onset of the study; another 733 reported a prior history of supplementation. After tracking the women for an average of nearly 11 years, researchers found that the risk of heart disease death was 31% lower in those taking vitamin D at the time of the study (Mercola 2002b).
Recent studies indicate that moderate or severe hypovitaminosis D was present in 66% of patients taking daily vitamin D in amounts less than the recommended dosage for their age; 37% of the patients taking daily vitamin D in excess of the recommended amount for their age were nonetheless still deficient. Thus, experts recommend at least 400 IU of vitamin D a day; if the individual is elderly and not participating in outdoor activities (and sunlight exposure), 800 IU a day is recommended (Thomas et al. 2000).
Vitamin E-- prevents plaque formation, protects LDL from oxidation, strengthens blood vessels, reduces blood viscosity and platelet aggregation, is helpful in atrial and ventricular fibrillation, is an antioxidant and antidiabetic nutrient, improves insulin sensitivity, is protective to smokers, reduces C-reactive protein, has diuretic activity, and is beneficial to those with hemochromatosis
In 1974, Dr. Passwater enrolled 17,894 persons (ages 50-98) in a study to determine the effects of long-term vitamin E supplementation. He found the length of time the individual used vitamin E was more important than the amount of the nutrient used. The trend was especially apparent beyond 9 years of usage. Taking 400 IU of vitamin E daily for 10 years or more strikingly reduced the occurrence of heart disease prior to 80 years of age (Passwater 1977).
An ongoing study involving 87,245 nurses (ages 34-59) and 39,910 male health professionals (ages 40-75) showed a significant relationship between the use of vitamin E supplements and a reduced risk of heart disease (Rimm et al.1993; Stampfer et al. 1993). A study reported in The Lancet may have eclipsed all others, showing that 2002 individuals with documented heart disease (supplemented with 400-800 IU of vitamin E daily) reduced their risk of nonfatal heart attacks 77% (Stephens 1996; Challem 2001).
These dramatic results occur in part because vitamin E prevents white blood cells from adhering to arterial walls. When monocytes are suppressed from bonding to the artery, a primary step in arterial closure has been averted (Devaraj et al. 2000a).
According to researchers at Georgetown University Medical School, vitamin E also renders the blood less sticky and platelets less prone to clump. In animal models of endothelial dysfunction, vitamin E improved the activity of endothelium-derived nitric oxide; this effect was not dependent upon the antioxidant protection of LDL cholesterol. Instead, it appears vitamin E inhibits platelet aggregation through a mechanism that involves protein kinase C inhibition, not its antioxidant activity as previously suspected (Freedman et al. 2001).
French scientists found that alpha-tocopherol supplementation prevented lethal ventricular arrhythmias associated with ischemia and reperfusion. In addition, animals with coronary arteries occluded for experimentation experienced a significant decrease in the ventricular fibrillation threshold; animals similarly occluded, but vitamin E supplemented, realized no decrease in the threshold (Dzhaparidze et al. 1986; Fuenmayor et al. 1989; Sebbag et al. 1994). Comment: Ventricular tachycardia represents at least three consecutive ventricular complexes with a heart rate of more than 100 beats a minute. Ventricular fibrillation is a cardiac arrhythmia marked by rapid, disorganized depolarizations of the ventricular myocardium. Blood pressure falls to zero, resulting in unconsciousness; without defibrillation and resuscitation, death can promptly ensue.
According to Ron Kennedy, M.D., atrial fibrillation is a condition in which the regular pumping function of the atria is replaced by a disorganized, ineffective quivering caused by the chaotic conduction of electrical signals through the upper chambers of the heart. The patient has various corrective options, including antiarrhythmic drugs, anticoagulants, radio-frequency ablation, a pacemaker, and, according to Dr. Kennedy, high-dose (2000 IU a day) vitamin E. Recall that vitamin E reduces blood viscosity and platelet aggregation. If the patient is receiving anticoagulant therapy and wishes to add vitamin E, close monitoring by a physician is essential to avoid compromising the clotting mechanism (Kennedy 1999).
Researchers from the University of Naples reported encouraging data regarding pharmacological doses (about 900 mg a day) of vitamin E administered to elderly patients with coronary heart disease and insulin resistance. Lower fasting and 2-hour blood glucose levels, reduced plasma insulin and triglyceride concentrations, and an improved HDL-LDL ratio indicate vitamin E is useful in stabilizing insulin-resistant patients with coronary heart disease (Paolisso et al. 1995).
According to Dr. Ishwarlal Jialal and Dr. Sridevi Deveraj, diabetics have increased inflammation and are more prone to cardiovascular disease (Deveraj et al. 2000). It appears that vitamin E, by decreasing inflammation, may contribute to a reduction in cardiovascular disease in both diabetic and nondiabetic subjects. Vitamin E lowered levels of IL-6 50%; 1200 IU of vitamin E reduced C-reactive protein (CRP) 30% (Devaraj et al. 2000b; O'Brien 2001). CRP levels remained constant 2 months postsupplementation. For an in-depth review of CRP, consult the CRP subsection under the sections Newer Risk Factors and The Link Between Infections and Inflammation in Heart Disease, in this protocol.
Vitamin E appears to be decreased in patients with hereditary hemochromatosis or iron overload. Iron loading, in experimental studies, significantly decreases hepatic and plasma vitamin E, a shortage amenable with supplementation. Free-radical index markers increase three- to fivefold in an iron-loaded liver, but supplementation with vitamin E has been shown to reduce levels by about 50% (Brown et al. 1996).
Free radicals activate a gene that encourages overgrowth of smooth muscles in the blood vessel walls, a process that can contribute to closure (Gonzalez-Flecha 2002). Vitamin E, a reliable antioxidant, has the opposite effect, that is, it turns off the gene responsible for smooth muscle proliferation. Vitamin E's antioxidant powers extend to protect the cells and organs (particularly the lungs) from damage caused by smoking.
Vitamin E has (for decades) been credited with diuretic activity, stimulating urine excretion (Davis 1965). This action is of a significant advantage to patients with edematous tissues and elevated blood pressure.
The type and blend of vitamin E used affects the end results. Studies have shown that alpha-tocopherol may not protect as aggressively against coronary heart disease unless it is combined with the gamma-tocopherol form. Both alpha-tocopherol and gamma-tocopherol can decrease platelet aggregation, inhibit blood clot formation, protect LDL cholesterol against oxidation, and increase endogenous SOD production (an enzyme with antioxidant activity); gamma-tocopherol, however, shows greater activity on each function.
Unfortunately, gamma-tocopherol has a couple of factors working against its utilization. For example, gamma-tocopherol can be obtained from foodstuffs, but it is poorly retained, and much of it is excreted in urine after being metabolized by the liver. Furthermore, a protein, referred to as alpha-tocopherol transfer protein, identifies and selectively chooses alpha-tocopherol over other forms of vitamin E. As a result, alpha-tocopherol is found more abundantly in lipids, blood, and body tissues.
It is strongly recommended that individuals relying upon the cardioprotective effects of vitamin E include the gamma-tocopherol form, but the complexing process determines the benefit. A union of alpha-tocopherol (80%) with gamma-tocopherol (20%) appears ideal; too much alpha-tocopherol may oppose the antioxidant qualities of gamma-tocopherol.
In addition, the hypolipidemic value of tocotrienols, the lesser known half of vitamin E, should not be overlooked. The most dramatic cholesterol reduction is seen when tocotrienol supplements are combined with dietary changes (a high-fiber, low-fat diet). In a 12-week, double-blind trial, those who responded to tocotrienol therapy saw a reduction of approximately 23% in total cholesterol and 32% in LDL cholesterol using dietary modification plus tocotrienol supplements. Tocotrienols alone yielded a 16% decrease in total cholesterol and a 21% decrease in LDL cholesterol (Quereshi et al. 1993; ACCM 1998). apo-B, a protein component found in LDL, VLDL, and IDL cholesterol also appears to be tocotrienol responsive (Qureshi et al. 1997).
Tocotrienols degrade the enzyme 3-hydroxy-3-methylgulutaryl coenzyme A reductase, a rate-limiting enzyme that participates in cholesterol synthesis. Researchers credited this function as being the mechanism delivering tocotrienol's hypolipidemic edge (Qureshi et al. 2001). A team of researchers from Switzerland reported greater hypolipidemic value when using gamma-tocotrienol rather than a mixture of tocotrienols (Raederstorff et al. 2002). To read more about tocotrienols and dosing recommendations, please consult the Tocotrienols subsection appearing earlier in this section.
A suggested dosage of vitamin E is 400-1200 IU a day. Comment: Initially, blood pressure rose in approximately one-third of hypertensive individuals treated with vitamin E (Shute 1976). Therefore, individuals who are hypertensive should use 100 IU a day for 1 month and add 100 IU each month until 400 IU a day is reached (Balch et al. 1997). Because of the reductions in blood glucose levels, diabetic individuals wishing to use vitamin E should begin with low dosages. Gradually increase the dosage, allowing for appropriate insulin or drug adjustments.
Reader's guide to vitamin E food sources, enhancers, and antagonists: Vitamin E is found in wheat germ, whole grains (brown rice, cornmeal, oatmeal, and wheat), vegetable oils (soybean, corn, and cottonseed), egg yolk, butter, milk fat, meat (especially liver), dark green leafy vegetables, legumes, nuts, and seeds.
Vitamin E enhancers are vitamin A, B complex vitamins, vitamin C, magnesium, manganese, selenium, inositol, and essential fatty acids. For optimal vitamin E absorption, excessive fat intake should be avoided, as well as birth control pills and the chronic use of mineral oil.
Vitamin K-- modulates calcium levels; reduces inflammation, C-reactive protein (CRP), IL-6, the risk of thrombosis, and the progression to valvular stenosis; and has a role in glucose management
As important as calcium is as a hypotensive and antiarrhythmic mineral, it has a detrimental side if it seeps into arteries. Arterial calcification, common to the aging process, is a risk factor leading to the development of heart disease, atherosclerosis, and mitral and aortic valve stenosis. Researchers recently reported the results of a comprehensive study evaluating 2213 individuals over a 10.4-year period in regard to coronary calcium levels. Those with a calcium score in the fourth quartile were 3.7 times more likely to die over the 10 years than were individuals in the first quartile (Buenano et al. 2000).
Harvard Medical School announced that about 25% of adults over 65 years of age have arterial calcification, increasing their risk of severe heart disease 50% (Harvard Heart Letter 1999). However, the Framingham Heart Study determined that the risks imposed by thoracic aortic calcification are not restricted to senior subjects; 35-year-old men with aortic calcification had 7 times the risk of dying of a sudden heart attack (Witteman et al. 1990).
The cumulative results of 8 years of research determined that women with severe kyphosis (increased convexity in the curvature of the thoracic spine) increased their risk of pulmonary death (likely a blood clot) by 2.6 times. Compared with women who were fracture-free, those with one or more vertebral fractures had a 1.23 times greater mortality rate. Mortality increased as the number of fractures increased (Kado et al. 1999).
It was also noted that women with atherosclerotic calcification had 7% less bone mass. Dutch researchers connected the dots and determined that postmenopausal women with calcification in bone tissue and atherosclerotic vessels had diminished vitamin K levels. It was concluded that vitamin K status affects the mineralization process in both bone and atherosclerotic plaque (Jie et al. 1996).
Vitamin K, an underutilized fat-soluble vitamin, overcomes the pathological effects of a calcium imbalance by promoting the deposition of calcium in its primary site (bone) and out of arterial walls.
Note: Because of the number of individuals using anticoagulants, it is important to note that warfarin (Coumadin) caused extensive arterial calcification in laboratory animals (Howe et al. 2000). Humans on long-term warfarin therapy may be at an increased risk for developing arterial calcification due to a drug-induced vitamin K deficiency.
So interrelated is bone loss to cardiovascular disease that measuring bone density has become a predictive factor for cardiovascular health. If bone density deviates one standard from the norm, the risk of stroke increases 3 times (Mitchell 2000). Vitamin K thus emerges as a star player in cardiovascular health, keeping calcium in bones and out of arteries and valves.
Note: Be aware that the risks imposed by low bone density have no gender preference. Low bone density is a strong and independent predictor of all-cause and cardiovascular mortality in both men and women (Trivedi et al. 2001).
A group of animals with induced atherosclerosis were given vitamin K (100 mg/kg of body weight), vitamin E (40mg/kg), or a placebo to assess reversal of the atherosclerotic process. At the conclusion of the study, the control group showed aortic calcium of 17.5 microns/mg; those receiving vitamin K had approximately 1 micron/mg of calcium, and vitamin E reduced it even further (Seyama et al. 1999) (for more information relating to valvular calcification, consult the section devoted to Valvular Disease in this protocol).
With age, the levels of IL-6 increase. This creates an imbalance between anti-inflammatory and pro-inflammatory cytokines (Ferrucci et al. 1999). Disproportionate numbers of good and bad cytokines increase inflammation, as well as bone degradation.
IL-6 is germane to this untoward sequence, promoting not only the inflammatory process, but also bone resorption, that is, the loss of substance from the skeletal system (Paule 2001). Vitamin K reduces the levels of IL-6; subsequently, the assault targeted at bone, as well as inflammation (a risk factor for both cardiovascular disease and cancer) is reduced (Reddi et al. 1995). Since C-reactive protein (CRP) is synthesized in response to IL-6, it appears vitamin K may be valuable in reducing elevations in CRP, as well.
Japanese researchers also found that a vitamin K deficiency can mimic the symptoms of diabetes. (The pancreas, which produces insulin, has the second highest levels of vitamin K in the body.) Low levels of vitamin K appear to induce a tendency toward a poor early insulin response and late hyperinsulinemia, following a glucose load in laboratory animals (Sakamoto et al. 1999). Lastly, vitamin K's antioxidant powers are rated (by some) as superior to either vitamin E or coenzyme Q10, other highly respected free-radical fighters (Mukai et al. 1993).
Typically, vitamin K would not be indicated if a patient is on anticoagulant therapy. However, The Lancet reported that asymptomatic patients on warfarin should consider low-dose vitamin K if blood-clotting time, as measured by the international normalized ratio (INR), is 4.5-10.0 (Crowther et al. 2000). Follow-up studies to determine the success of vitamin K therapy (1 mg a day) showed that 4% of the patients who received vitamin K therapy had bleeding episodes, compared with 17% of those in the placebo group. The conclusion of the study was that low-dose vitamin K, an inexpensive intervention without known toxicity, might prevent a hemorrhage in patients on warfarin therapy.
A suggested vitamin K dosage for patients not on anticoagulant therapy is 10 mg a day.
Reader's guide to vitamin K food sources and antagonists: Friendly bacteria in the intestines synthesize the majority of vitamin K. However, persistent low-grade levels of intestinal bacteria in the small intestine could hamper vitamin K synthesis. Acidophilus cultures in the form of yogurt or kefir serve not only as a good food source, but also ensure that sufficient friendly intestinal flora are present for vitamin K production.
Green leafy vegetables are vitamin K-rich; other sources include alfalfa, egg yolks, blackstrap molasses, asparagus, Brussels sprouts, cauliflower, oatmeal, and rye. Antibiotics increase the need for vitamin K, and vitamin E (doses greater than 600 IU) antagonizes vitamin K activity.
The calcium paradox
It is important to look at the ways calcium can become an atheromatous material. Most body stores of calcium are found in the bones and teeth, and 1% is found in the bloodstream. This 1% performs so many vital functions, including cardiac health, that the body vigorously defends this minute percentage. If inadequate calcium is available, vitamin D is mobilized in the kidney and rushes to the intestinal wall to pull more calcium into the bloodstream. If inadequate amounts of vitamin D are available, the parathyroid gland delivers a message to bones to release calcium. Because the calcium mass in the bone is so great, it is easy for too much of the mineral to be extracted, overwhelming the amount needed in the blood. After compensating for deficiencies, the excess calcium ties up in soft tissues, the lining of arteries, and brain tissue.
Poor calcium regulation also affects arterial plaque, causing it to become harder but more brittle (Harvard Heart Letter 1999). This occurs as calcium deposits in the blood attach to cholesterol deposits on the walls of arteries, making an almost impenetrable union (Shappell 2000). This process further narrows the artery, causing symptoms ranging from fainting spells to sudden death due to abrupt changes in blood pressure (Doss 2001).
It is important to grasp that excesses of calcium (potentiating arterial disease) come essentially from the bone. Furthermore, the results of a test indicating adequat