THROMBOTIC RISK FACTORS
Homocysteine is a toxic compound formed in the body from the amino acid methionine. Several studies have shown that homocysteine increases blood coagulation by inhibiting tissue fibrinogen activators. The result is increased levels of fibrinogen and fibrin (de Jong et al. 1998; Selhub et al. 1998; Coppola et al. 2000; Durand et al. 2001; Kuch et al. 2001).
In order to reduce blood homocysteine levels, adequate amounts of folic acid, vitamin B12, and vitamin B6 are usually required. High homocysteine levels have been shown to be a risk factor for cardiovascular disease, including atherosclerosis, heart attack, and stroke. Ideal levels of homocysteine are under 7 micromoles/L of blood.
Fibrinogen is the precursor to fibrin, a coagulant protein that binds platelets together to form a blood clot. It has a role in normal and abnormal clot formation (coagulation) in the body. During coagulation, fibrinogen reacts with thrombin, releasing four small fibrinopeptides that produce fibrin, which in turn creates an insoluble fibrin network generally referred to as a scab.
Fibrinogen also participates in the cellular phase of coagulation. Fibrinogen promotes platelet aggregation, which can lead to diminished blood flow and reduced delivery of oxygen to the body. Fibrinogen can also cause blood platelets to bind together, initiating abnormal arterial blood clots.
An article in the journal Neurology described a study of cardiovascular laboratory tests in 136 patients with acute stroke, 76 patients with comparable risk factors for stroke, and 48 healthy controls. Statistical analysis found that prior stroke and fibrinogen levels predicted new events in stroke patients. After 1 year, fibrinogen levels remained elevated in stroke survivors. The researchers concluded that fibrinogen levels are associated with increased risk of recurrent vascular events (Beamer et al. 1998).
The Life Extension Foundation recommends the measurement of fibrinogen as part of a cardiovascular risk assessment. The normal reference range for fibrinogen is 200-400 mg/dL. Optimally, fibrinogen should be 200-300 mg/dL.
Once symptomatic atherosclerosis has developed, a person is at significant risk for stroke, heart attack, and peripheral arterial occlusion. The occlusive event (stroke, MI, etc.) tends to develop at sites of preexisting narrowing (stenosis). Atherosclerotic plaques can rupture and expose tissue factor-rich plaque contents to the blood, initiating thrombus formation.
Chronic inflammation is associated with a variety of chronic diseases, including cardiovascular disease. C-reactive protein (CRP) is a sensitive indicator of inflammation that rises before the erythrocyte sedimentation rate. CRP is a marker of systemic inflammation and unstable arterial plaque, both of which are indictors of increased thrombotic risk. Certain pro-inflammatory immune cytokines cause elevated CRP. These cytokines may be suppressed by taking supplements such as the DHA fraction of fish oil, the hormone DHEA, vitamin K, and nettle leaf extract.
An article in the journal Thrombosis Research described a study of patients with acute thrombotic stroke prior to treatment. The patients with elevated CRP also had significantly elevated plasma levels of thrombin-antithrombin complex, plasmin-antiplasmin complex, and d-dimer of fibrin. When compared to those with normal levels, platelet aggregation induced by ADP was also significantly higher in patients with elevated CRP. The authors hypothesized that the activation of the blood coagulation and platelet aggregation system may be related to elevated CRP levels in stroke patients (Tohgi et al. 2000). A feature article in the May 2002 issue of Scientific American further emphasized the link between chronic inflammation and the evolution of atherosclerosis and coronary artery disease (Libby 2002).
Measuring CRP levels (using a high-sensitivity C-reactive protein blood test) is highly recommended by the Life Extension Foundation.
Lipoprotein(a) is an altered form of LDL cholesterol that has a structure nearly identical to plasminogen, a protein that forms plasmin. Plasmin dissolves fibrin. Unfortunately, lipoprotein(a) inhibits the breakdown of fibrin by competing with plasminogen. Lipoprotein(a) was found to be a key component in blood clots, plaque formation and coronary heart disease (CHD) (Rath et al. 1989; Beisiegel et al. 1990).
Linus Pauling's theory of heart disease focused on the adverse effects of lipoprotein(a) on the cardiovascular system. Pauling and Rath proposed that lipoprotein(a) acted as a surrogate (replacement) for vitamin C (Rath et al. 1990a). They also proposed that a deficiency of vitamin C resulted in the increased production of lipoprotein(a), which both hardened the arteries and caused blood clots (Rath et al. 1990b). Linus Pauling recommended the use of high doses of pure vitamin C and lysine to both prevent and treat cardiovascular disease. Niacin, CoQ10, serine, and regular aerobic exercise have also been shown to lower lipoprotein(a) (Cohn 1998; Singh et al. 1999; Batiste et al. 2002).
The endocrine system is a complex mechanism in which each organ impacts the function of other organs. A low-functioning thyroid (hypothyroidism) would therefore impact other systems, including the cardiovascular system. Hypothyroidism is associated with increased cholesterol levels, atherosclerosis, and increased homocysteine (Carantoni et al. 1997; Diekman et al. 1998; Nedrebo et al. 1998; Hussein et al. 1999; Hak et al. 2000; Kahaly 2000; Diekman et al. 2001). The effect of hypothyroidism on the blood clotting system is currently controversial and is the focus of several studies (Chadarevian et al. 1998; Muller et al. 2001).
COMPREHENSIVE LABORATORY TESTING FOR CARDIOVASCULAR RISK
The Life Extension Foundation recommends that all of its members be checked for cardiovascular risk with both conventional laboratory tests and new markers such as CRP.
Standard Reference Ranges and Optimal Levels
Blood Test - Standard Reference Range - Optimal Levels
Cholesterol - 100-199 mg/dL - 180-200 mg/dL
LDL cholesterol - 0-129 mg/dL - Under 100 mg/dL
HDL cholesterol - 35-150 mg/dL - 55-150 mg/dL
Triglycerides - 0-199 mg/dL - 40-100 mg/dL
Glucose - 65-109 mg/dL - 70-100 mg/dL
Homocysteine - 5-15 micromol/L - Under 7.0 micromol/L
Fibrinogen - 200-460 mg/dL - 200-300 mg/dL
CRP - Up to 4.9 mg/L - Under 2 mg/L; preferably under 1.3 mg/L
Furthermore, optimal ranges of these laboratory tests are much narrower than the standard reference ranges used in conventional medicine. It is important to emphasize that the "average" person has a high risk of developing a thrombotic-related disease. For health-conscious people, this dismal fate is unacceptable.
CONSULTING YOUR PHYSICIAN
When over-the-counter supplements, such as aspirin, vitamins, herbs, and oils are used as primary antithrombotic therapy, the risk of undesirable side effects is reduced significantly. However, although over-the-counter medications such as aspirin and natural therapies come with a lower risk of hemorrhaging, they should not be substituted for prescription medication if you are at a high risk for thrombosis. Some common conditions that cause a high risk of thrombosis include atrial fibrillation, valvular replacement, recurrent or chronic deep venous thrombosis, pulmonary embolism, and cancer.
Because appropriate therapeutic dosing is crucial and the associated risks can be life-threatening in all circumstances that require anticoagulation therapy or antiplatelet therapy, your physician must be consulted if you desire to make any substitutions to your medication. Because medications, such as Coumadin and heparin, have very narrow therapeutic ranges, anyone on these medications should have his or her blood tested frequently for prothrombin using the INR as a reference range. Once the effective dose is achieved, blood testing is recommended every 1-2 weeks to monitor the medication blood levels and to avoid overdosing, which could lead to hemorrhaging. In addition to the INR values, template bleeding time should also be closely monitored if any over-the-counter drugs or natural supplements that affect the clotting cascade are added to the regimen. Some of these supplements include vitamin E, ginkgo biloba, CoQ10, garlic, ginseng, green tea, vitamin C, vitamin A, policosanol, Dong Quai, white willow, ipriflavone, and vinpocetine (periwinkle).
* Cholesterol-Lowering Supplements
* Natural Platelet Aggregation Inhibitors
* Lowering Homocysteine
* Sulfur-Containing Compounds
The nutritional supplements listed below have been scientifically studied specifically for their ability to reduce the risk of thrombosis. The bulk of the research focuses on inhibiting platelet aggregation. The supplements are divided into several broad categories based on their primary actions:
* Cholesterol-lowering supplements
* Natural platelet aggregation inhibitors
* Homocysteine-lowering supplements
* Sulfur-containing compounds
Note: The supplements in the natural blood thinners category could easily have been put into other categories. Ginkgo and vitamin E, for instance, are very powerful antioxidants. Essential fatty acids are also known for their anti-inflammatory actions. However, their blood-thinning effects are much more important in the prevention of thrombosis.
Policosanol is a cholesterol-lowering agent derived from sugar cane wax. In some cases, it can normalize cholesterol, as well as prescription drugs, doing so without side effects.
The efficacy and safety of policosanol has been shown in numerous clinical trials. It has been used by millions of people in other countries. Policosanol can lower LDL cholesterol as much as 20% and raise protective HDL cholesterol by 10%. This compares favorably with some cholesterol-lowering drugs that can cause side effects such as liver dysfunction and muscle atrophy (Mas et al. 1999).
Policosanol works by blocking the synthesis of cholesterol. It may not inhibit the HMG-CoA enzyme like the "statin" cholesterol-lowering drugs. Instead, it may inhibit a different enzyme involved in cholesterol synthesis. However, its exact mechanism is not known. Like statin drugs, policosanol helps stop the formation of atherosclerotic lesions, which was proven in studies using rabbits fed a diet designed to create high cholesterol (Noa et al. 1995).
Policosanol inhibits the formation of clots and may work synergistically with aspirin in this respect. In a comparison of aspirin and policosanol, aspirin was better at reducing one type of platelet aggregation (clumping together of blood cells) and policosanol was better at inhibiting another type. Together, policosanol and aspirin worked better than either one alone (Arruzazabala et al. 1997; Stusser et al. 1998).
An article in the journal Pharmacology Research described a randomized, double-blind, placebo-controlled study of policosanal and aspirin. Participants received either policosanol (20 mg daily), aspirin (100 mg daily), a combination of both, or placebo for 7 days. The effects on platelet aggregation are summarized above (Arruzazabala et al. 1997). A related effect is that significant reductions in the level of thromboxane (a blood vessel-constricting eicosanoid produced by platelets) occur in humans after 2 weeks of policosanol (Carbajal et al. 1998).
The normal dose of policosanol is 10-20 mg taken at bedtime. Cholesterol levels should be measured regularly because both high and low cholesterol levels are considered unhealthy. Consider using aspirin (81 mg daily) in combination with policosanol.
Aged garlic has become a well-known, popular supplement for the cardiovascular system. Garlic has been found to increase the synthesis of nitric oxide, a chemical messenger that inhibits platelet aggregation and vasodilates blood vessels (Das et al. 1995; Dirsch et al. 1998; Kim-Park et al. 2000; Kim et al. 2001).
An article in the journal Nutrition described a randomized, double-blind study of aged garlic on normal, healthy individuals. The researchers found that aged garlic inhibited platelet adherence and aggregation. Higher doses (7.2 grams daily) had a more profound effect than lower doses (2.4 grams daily) (Steiner et al. 2001).
The specific effects of aged garlic have been the subject of several studies. Aged garlic has been shown to inhibit platelet aggregation by ADP, epinephrine, and collagen, although one study found that it did not affect ADP-induced aggregation (Steiner et al. 1998; Rahman et al. 2000).
Another study examined the effects of consuming one fresh clove of garlic every day on men. After 26 weeks of garlic consumption, there was an approximate 20% reduction of serum cholesterol and about 80% reduction in serum thromboxane B2, a stable metabolite of thromboxane A2. Recall that thromboxane A2 is a platelet aggregator and vasoconstrictor secreted by platelets (Ali et al. 1990, 1995).
Niacin (vitamin B3) causes peripheral vasodilation (flushing) within about 20 minutes. Large doses of niacin (up to 6 grams daily) have been found to lower cholesterol, raise HDL, and lower LDL and VLDL lipids. The safest form of niacin is inositol hexa-nicotinate in the dose of 1600-2400 mg daily. Individuals taking continuous high-dose niacin therapy need to have their blood levels monitored for elevations in liver enzymes and uric acid.
An article in the American Heart Journal described the Arterial Disease Multiple Intervention Trial (ADMIT), a multicenter, randomized, placebo-controlled trial to assess the feasibility of an antioxidant therapy on coagulation. Patients with peripheral artery disease randomly received low-dose Coumadin, niacin, an antioxidant vitamin cocktail, or placebo. Unexpectedly, the niacin treatment resulted in a significant decrease in fibrinogen (Chesney et al. 2000).
Natural Platelet Aggregation Inhibitors
Ginkgo biloba extract is made from the leaves of the oldest living tree. Ginkgo biloba has a long history of medicinal use. It has become a very popular herb to help improve memory, particularly in the elderly.
Ginkgo biloba has been shown to inhibit platelet aggregation induced by platelet-activating factor (PAF), but not by oxidative stress (Akiba et al. 1998).
An article in the journal Thrombosis Research described a study of the effects of ginkgo biloba in combination with ticlopidine when used to treat rats with experimentally induced thrombosis. The combination of ginkgo biloba (40 mg/kg daily) and a small dose of ticlopidine (50 mg/kg daily) was shown to be comparable to a large dose of only ticlopidine (200 mg/kg daily). The combination also prolonged bleeding time by 150% and consistently decreased the thrombus weight (Kim et al. 1998).
Essential Fatty Acids
Essential fatty acids are found in healthy oils, such as flax, borage, perilla, and fish oils. Essential fatty acids are termed "essential" because they are necessary for life. Essential fatty acids, including DHA (docosahexaenoic acid) and EPA (eicosapentaenoic acid), are known to inhibit platelet aggregation and are included as potential contraindications for use with anticoagulant (warfarin) therapy. The contraindication is actually more of a strong caution to avoid thinning the blood too much. What this means is that if a patient on Coumadin does take fish oil supplements, the TBT test should be done in addition to checking the INR reference range.
Several studies examined the antiplatelet mechanisms of essential fatty acids like EPA and DHA and showed they inhibited collagen- and arachidonic acid-induced platelet aggregation. No effects were seen in thrombin-induced aggregation. The mechanism was related to the ability of these fatty acids to suppress thromboxane A2 formation by inhibiting cyclooxygenase-1 (Ikeda et al. 1998; Akiba et al. 2000).
An Australian study found that omega-3 fatty acids (those rich in alpha-linolenic acid, such as flaxseed and perilla oils) were more effective than omega-6 fatty acids (those rich in linoleic acid, such as sunflower oil) (Allman et al. 1995). This same result was also reported in a German study which found that an omega-3 to omega-6 ratio of 15:1 caused a significant decrease of collagen-induced platelet aggregation (Stroh et al. 1991).
Vitamin E (tocopherol) is a potent antioxidant that has been shown to increase prostaglandin I2 synthesis, one of the platelet aggregation inhibitors and vasodilators. Vitamin E is depleted by estrogen, birth control pills, and chlorine.
A study found that vitamin E was able to inhibit collagen-induced platelet aggregation at concentrations achievable in blood after supplementation. The researchers also isolated a mechanism by which vitamin E blunts hydrogen peroxide formation, which then mediates arachidonic acid metabolism and phospholipase C activation in platelet aggregation induced by collagen (Pignatelli et al. 1999).
Caution: If vitamin E is used with Coumadin, the template bleeding time test should be done by the physician to guard against risk of hemorrhage.
Vitamin K plays a unique role in the clotting system by contributing to both coagulation and anticoagulation. Vitamin K is a precursor of coagulation factors II, VII, IX, and X. Vitamin K is also a cofactor for the synthesis of proteins C and S. Protein C is a proteolytic enzyme that acts as an anticoagulant by inactivating clotting factors V and VIII and by increasing production of tissue plasminogen activator.
An article in the journal Lancet recommended that asymptomatic patients on Coumadin should consider low-dose vitamin K if blood-clotting time, as measured by the INR, is 4.5-10.0. The article described a multicenter, double-blind, placebo-controlled, randomized trial in which patients received either a placebo or 1 mg of vitamin K orally. Patients given vitamin K had a more rapid decrease in the INR than those given placebo, and fewer of them had bleeding episodes during the follow-up period. The authors concluded that low-dose vitamin K therapy rapidly lowers INR values in patients taking Coumadin and may be effective in preventing hemorrhage (one of the common side effects of Coumadin therapy) (Crowther et al. 1998, 2000).
Vitamin K counteracts the action of Coumadin and is strictly contraindicated in patients on anticoagulant drug therapy. The Life Extension Foundation recommends the use of 10 mg daily of vitamin K in healthy individuals.
Homocysteine has slowly become accepted in conventional medicine as a risk factor for cardiovascular disease. Clinical research has shown that some vitamins (folic acid and vitamins B6 and B12) are very effective at lowering homocysteine levels. It has been proposed that homocysteine activates the blood clotting system by damaging endothelial cells.
An article in Thrombosis Research described a study of 11 persons with high homocysteine levels who had atherosclerosis. After an 8-week treatment with folic acid (5 mg daily, orally), vitamin B6 (300 mg daily, orally), and vitamin B12 (1000 mcg weekly, intramuscularly), homocysteine levels dropped from an average of 20 to 10. Vitamin treatment was also associated with a significant decrease in the markers of thrombin formation, including thrombin-antithrombin III complexes and prothrombin fragment 1+2 concentrations in peripheral venous blood. Bleeding time became prolonged by about 60 seconds (Undas et al. 1999).
The Life Extension Foundation strongly recommends that homocysteine levels be measured. Supplementation with vitamins B6 and B12 and folic acid are recommended to lower homocysteine levels.
Curcumin is the Latin name for the common yellow spice known as turmeric. Curcumin is commonly used for its anti-inflammatory effects. Curcumin has also been shown to lower cholesterol.
Research has examined the mechanism of the antiplatelet action of curcumin (turmeric). Curcumin was shown to inhibit platelet aggregation induced by ephedrine, ADP, platelet-activating factor (PAF), collagen, and arachidonic acid. Curcumin acted most strongly against aggregation by PAF and arachidonic acid. The mechanism appeared to be related to curcumin's inhibition of thromboxane A2 (Shah et al. 1999). Curcumin should be taken with meals to avoid the possibility of gastric irritation. The daily dose for most people is 900 mg with 5 mg of bioperine to enhance assimilation.
DHEA has been shown to inhibit inflammatory cytokines (Straub et al. 2000). With reduced inflammation, less platelet aggregation and LDL migration into the vessel walls occurs. This can lead to less thrombus formation and atherosclerosis. DHEA also competitively inhibits cortisol, the other main adrenal steroid (Boudarene et al. 2002). If cortisol levels are high, DHEA may be depleted leading to immune deficiencies and reduced muscle mass. High cortisol also worsens responses to stress.
Nettle Leaf (Urtica Dioica)
In Germany, nettle leaf is an herb with a long tradition of use as an adjuvant remedy in the treatment of arthritis. It has also been used extensively in the treatment of allergies. Nettle leaf extract has been found to contain a variety of active compounds, such as cyclooxygenase and lipoxygenase inhibitors, and substances that affect cytokine secretion (Obertreis et al. 1996a; 1996b; Teucher et al. 1996).
Cytokines are proteins that carry messages between cells and regulate immunity and inflammation. Two cytokines, tumor necrosis factor alpha (TNF-a) and interleukin-one-beta (IL-1b), are examples of pro-inflammatory cytokines (Pinto et al. 1999). These cytokines have been found to be elevated in patients with allergies and arthritis. In animal models, it was shown that inhibition of TNF-a results in decreased inflammation, while inhibition of IL-1b effectively prevents cartilage destruction (Probert et al. 1995).
Nettle leaf reduces TNF-a levels by potently inhibiting the genetic transcription factor that activates IL-lb and TNF-a. This pro-inflammatory transcription factor, nuclear factor kappa beta ( NF-kb), is known to be elevated in chronic inflammatory diseases and is essential to activation of TNF-a. Nettle leaf is also thought to work by preventing degradation of the natural inhibitor of NF-kb in the body (Riehemann et al. 1999). In vessels, reduction of inflammatory cytokines (such as TNF-a) also reduces platelet aggregation and the tendencies toward thrombus formation.
Quercetin and Catechin
Quercetin and catechin (from green tea) are bioflavonoids with strong antioxidant properties. Quercetin is primarily used for its beneficial effects on allergies.
An article in the American Journal of Clinical Nutrition found that catechin and quercetin inhibited collagen-induced platelet adhesion. The authors proposed that the effects may be due to the ability of catechin and quercetin to decrease hydrogen peroxide production (Pignatelli et al. 2000). Quercetin may also inhibit platelet aggregation by its antioxidant properties (Xie et al. 1996).
Another study examined the inhibition of thrombin-induced platelet aggregation by a semisynthetic derivative of quercetin. The authors found that quercetin inhibited platelet aggregation by reducing calcium mobilization and influx (Liu et al. 1999, 2000).
Green tea has become very popular for the prevention and treatment of a wide range of diseases. Green tea protects the cardiovascular system and might prevent cancer.
A study in the journal Thrombosis Research examined the effects of green tea tannins and epigallocatechin on platelet aggregation. Both substances inhibited platelet aggregation induced by ADP and collagen in rats. They also inhibited platelet aggregation induced by ADP, collagen, and epinephrine in human blood samples (Kang et al. 1999).
In rabbits, Japanese researchers found that green tea inhibited aggregation of platelets. The researchers noted that epigallocatechin suppressed collagen-induced platelet aggregation. Epigallocatechin also inhibited platelet aggregation induced by thrombin and platelet-activating factor (PAF) (Sagesaka-Mitane et al. 1990).
Lycopene, found in tomatoes, has been shown to have strong antioxidant properties. Lycopene may be particularly effective in blocking the oxidation of LDL cholesterol.
An article in the journal Platelets described a study of fruits and their effect on human platelet aggregation in vitro. Researchers found that tomato extract inhibited both ADP- and collagen-induced aggregation by up to 70%. The antiplatelet components were found to be concentrated in the yellow fluid around the seeds in tomatoes. Grapefruit, melon, and strawberry were also found to have antiplatelet activity, but to a lesser extent (Dutta-Roy et al. 2001).
Grapes have gained popularity as a result of several studies that found that consuming 1 cup of red wine daily had beneficial effects on the cardiovascular system. Grapes contain proanthrocyanadins, which are concentrated in the seeds and skin and impart the blue color. Studies have shown that the antioxidant power of grape seed-skin extract is 50 times greater than vitamin E and 20 times greater than vitamin C.
An article in the journal Circulation described a study that examined the effects of purple grape juice on platelets. Laboratory tests (in vitro) found that purple grape juice inhibited platelet aggregation, increased nitric oxide production, and decreased superoxide formation. The researchers then conducted a study with 20 healthy subjects who consumed 7 mL/kg daily of purple grape juice for 14 days. Purple grape juice supplementation inhibited platelet aggregation, increased platelet nitric oxide production, and decreased superoxide formation. The authors proposed that purple grape juice may have beneficial effects in cardiovascular disease (Freedman et al. 2001).
An article in the journal Nutrition described a study in which 10 healthy subjects drank 5-7.5 mL/kg daily of purple grape juice, grapefruit juice, or orange juice for 1 week. Drinking purple grape juice reduced platelet aggregation by 77%. Orange and grapefruit juice had no effect. The authors proposed that the flavonoids in grape juice may decrease the risk of thrombosis (Keevil et al. 2000).
The amino acid N-acetyl-L-cysteine (NAC) inhibits platelet aggregation by several mechanisms, including:
* Increasing the antiplatelet aggregating effects of L-arginine, which promotes endogenous synthesis of nitric oxide (Anfossi et al. 1999, 2001). Increases in nitric oxide cause arterial vasodilation increasing blood flow to the heart and brain in coronary artery disease or cerebral ischemia. However, in doing so, nitric oxide generates the free radical nitric peroxide, which is best quenched by gamma tocopherol, a fraction of vitamin E. A recommended protocol for arterial vasodilation includes the use of gamma tocopherol (200-400 IU) in combination with L-arginine (1800-3600 mg) 2-4 times daily, and NAC (250 mg) 3 times daily. This combination may lower blood pressure as well.
* Affecting platelet-derived growth factor, a key player in fibrosis (Durante et al. 1999; Okuyama et al. 2001).
NAC is an antioxidant that is helpful in breaking up pulmonary and bronchial mucus. NAC is also a precursor of glutathione.
Onion juice has been shown to reduce in vitro human platelet aggregation. To retain their health benefits, onions should be eaten raw or lightly steamed because high heat deactivates the active ingredients.
The antiplatelet aggregation action of onions is attributed to sulfur compounds called thiosulfonates. The strongest thiosulfonates are allicin, propyl propane thiosulfonate, and ethyl ethane thiosulfonate. All three of these thiosulfonate compounds were shown to be significantly more potent platelet aggregators than aspirin at nearly equivalent doses (Briggs et al. 2000).
In a study using 9-week-old rats, the antithrombotic effects of Welsh onion juice was examined. Two days after treatment (2 g/kg daily), the raw Welsh onion juice consumption significantly lowered systolic blood pressure, prolonged bleeding time, and diminished platelet adhesion as compared to controls. The authors also found that boiled onion juice had no effect (Chen et al. 2000).
An article in the journal Nutrition described a study in dogs in which onion juice was administered 20 minutes after the coronary arteries were mechanically damaged (narrowed). Treatment with onion juice reversed the induced cyclic flow reduction within 2.5-3 hours in all five of the treated dogs. The authors concluded that onion juice might help prevent platelet-mediated cardiovascular disorders, but also noted that the effects might be greater in dogs than in humans (Briggs et al. 2001).
The effects of exercise on fibrinogen levels have been extensively studied. Several studies demonstrate that regular exercise lowers fibrinogen levels and reduces the risk of thrombosis (El-Sayed et al. 1999; 2000; Koenig et al. 2000; Imhof et al. 2001; Verissimo et al. 2001).
Regular exercise is also well known to provide a host of other health benefits, particularly for the cardiovascular system.
Prevention of blood clots is a complex task involving maintenance of a fine balance between the process of coagulation and anticoagulation. Patients on prescription medications (e.g., Coumadin), as well as those who combine Coumadin with over-the-counter anti-inflammatories or aspirin, need close monitoring, in particular weekly or biweekly testing of their prothrombin using the INR and the TBT test. Patients taking supplements (such as vitamins, herbs, or oils) should also have their thrombotic risk factors evaluated in the same way. However, close monitoring of coagulation balance is usually not necessary in people who are otherwise healthy.
Caution: Never change an anticoagulation medication without physician approval: thrombosis, bleeding, and sudden death can occur.
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