STROKE / thrombosis / phlebitis
Natural Prevention Strategies
Stroke
The term
"stroke" refers to a cerebrovascular accident (CVA) where the
brain is deprived of oxygen due to blood vessel blockage (80% of
strokes) OR the rupture of a blood vessel which causes
bleeding in the brain (20% of strokes). Either of these events
deprives areas of the brain of oxygen and can lead to neurological
damage. A transient ischemic attack (TIA) is a similar, smaller
event, resolving in minutes to hours and without permanent damage.
Recurrent TIA’s often precede a true stroke, and the causes of
both are the same. Stroke (Cerebrovascular disease) is the most
common cause of neurologic disability in Western countries.
Twenty percent of strokes are hemorrhagic, resulting from the
rupture of a cerebral artery. Causes of hemorrhagic stroke include
hypertension, aneurysm, blood vessel defects (inborn) and excess
blood-thinning medication.
The remaining eighty percent of strokes are due to blockages
resulting from emboli (a clump of blood cells or atherosclerotic
plaque) in a cranial artery. Causes of infarct stroke are
atherosclerosis, high blood pressure, excess blood-clotting
factors (see "conditions predisposing to blood clot formation,"
below), blood turbulence (due to arrhythmias, heart valve defects,
arteriovenous malformation, and atherosclerosis), diabetes, and
vascular inflammation.
A far lesser number of strokes may be due solely to lack of oxygen
without a blockage, usually due to sympathomimetic drugs (cocaine,
amphetamine), arterial compression caused by bone spurs, or
circulatory insufficiency due to decreased overall circulation.
Thrombosis
"Thrombosis" refers to a blood clot that develops in a
blood vessel. It is one of the leading causes of death in the
Western world.
If a thrombosis forms in a coronary artery, a myocardial
infarction may result. When thromboses form in the brain, the
resultant oxygen deprivation may result in TIA or stroke. An
emboli occurs when a clot breaks free and travels to other parts
of the body. If an emboli reaches the brain, again, stroke may
occur. Thromboses and emboli can also cause serious damage to
lungs, kidneys --- in fact, virtually
any organ.
Phlebitis /
Thrombophlebitis
"Thrombophlebitis," or deep venous thrombosis (DVT) is the
most common presenting vein disorder. Most vein clots begin in the
valves of deep calf veins. Tissue substances are released that in
turn form clumps of red blood cells (RBC’s). If these clumped
blood cells remain in the leg or elsewhere, they cause redness,
swelling, and pain. If they dislodge and travel to the brain, they
can cause a stroke.
Causes of venous thrombosis include:
1) Blood vessel lining injury (caused by catheters, septic
phlebitis, injection of irritating substances, trauma).
2) Excess blood clotting (due to malignant tumors, blood
cell abnormalities, oral contraceptives and inflammation).
3) Slowed blood flow (varicose veins, prolonged bed rest,
heart failure, dependent immobilization of the legs such as occurs
during car or air travel).
Factors which can cause blood clots
Specifically, any one of the following conditions may
predispose to blood clot formation:
- elevated homocysteine levels
- oxidized LDL cholesterol levels
- platelet activating factor (PAF)
- elevated fibrinogen
- elevated thromboxane A2,
prostaglandin E2, lipooxygenase, cyclooxygenase
- free-radical induced platelet
aggregation
- thrombin activating factor
- deficiency of tissue-plasminogen
activator (tPA)
- increased blood viscosity
- increased platelet count
- increased red blood cell kinase
activity
- inflammation of the arterial
wall
- atherosclerotic plaque
- elevated
triglycerides
- increased
platelet adhesion
- collagen-induced platelet
adhesion
- arachidonic acid-induced
platelet aggregation
- adenosine-induced platelet
aggregation
- epinephrine-induced platelet
aggregation
- serotonin-induced platelet
aggregation
- antigen-antibody reactions
- elevated thromboxane A2,
prostaglandin E2, lipooxygenase, cyclooxygenase
- free-radical induced platelet
aggregation
- thrombin activating factor
- deficiency of tissue-plasminogen
activator (tPA)
- increased blood viscosity
- increased platelet count
- increased red blood cell kinase
activity
- inflammation of the arterial
wall
- atherosclerotic plaque
- elevated triglycerides
- increased platelet adhesion
- collagen-induced platelet
adhesion
Fibrin thrombi can be prevented by
conventional anticoagulant therapy (heparin or coumarin
/ coumadin / warfarin compounds), but platelet aggregation
is not inhibited by these agents. (Merck Manual p. 586). It is
estimated that only 1/3 of all causative agents of thrombosis are
blocked by the administration of conventional blood thinning
drugs.
Treatment Considerations
Treatment of the underlying cause of thrombosis, and
phlebitis which results in thrombosis, are the mainstays of
prevention of stroke occurrence and reoccurrence. High
blood pressure, high cholesterol (especially with low HDL- the
"good" cholesterol), excessive blood clotting ("blood sludge"),
and atherosclerosis should be addressed as indicated.
Because of the many and varied causes of thrombosis, a
multi-faceted approach to anticoagulation and blood viscosity
normalization is surer than conventional anticoagulant (coumadin)
therapy alone.
DIET AND LIFESTYLE RECOMMENDATIONS
- Diet: eat a nutritious diet high
in nutrient-rich foods. Plant foods contain phytonutrients which
help prevent blood from clotting abnormally.
- Achieve and maintain a normal
weight.
-
Exercise
regularly. 30 minutes, 3 times per week minimum.
- Don’t smoke! Smoking irritates
the blood vessel lining and such irritation initiates a chain of
events that cause blood to clump.
- Drink 64 ounces of pure water
daily. Dehydration causes blood vessel irritation and can
predispose to abnormal blood clotting.
PRIMARY SUPPORT
-
Maxi Multi:
3 caps, 3 times per day with meals. Optimal (not minimal) doses
of antioxidant nutrients (vitamin A, beta carotene, C, E, zinc,
selenium), B6, B12, folic acid, bioflavonoids and magnesium are
especially important. Magnesium helps prevent high blood
pressure, a cause of stroke.
- Omega 3 fatty acids: the anti-inflammatory
action of Omega-3’s helps prevent blood vessel irritation.
Flax seed meal,
2 teaspoons per day with food
OR
Flax seed capsules:
2-4 caps, 3 times per day (target dose range: 6-12 caps per day)
OR
Flax seed oil:
1 tablespoon per day
OR
Max EPA
(Omega-3 rich fish oil): 1-2 caps, 3 times per day with meals
(target dose: 3-6 caps per day).
-
MAXI-GREENS: 3 caps, 3
times per day. Maxi greens contains a spectrum of the herbs
known to maintain normal blood viscosity. (grape seed, ginkgo,
bilberry, green tea).
ADDITIONAL SUPPORT
(Treat known risk factors.
Consult
an alternative medicine physician for further assistance):
High Cholesterol or Triglyceride levels:
Follow additional recommendations for
High Cholesterol
Diabetes (which predisposes to atherosclerosis):
Follow additional recommendations for
Diabetes
Atherosclerosis:
Follow additional recommendations for
Atherosclerosis
High fibrinogen:
Omega-3 oils,
garlic,
exercise,
niacin,
bromelain.
High homocysteine levels:
B6, B12 and folic acid. (NOTE: Maxi Multi contains optimal
doses of these nutrients. Take
additional B6, B12 and folic acid only if you are not taking Maxi
Multi,
MyPacks or the equivalent).
High ferritin (storage iron):
__________________________________________________________________________
Primary Materia Medica for Stroke Prevention
(Professional descriptions follow. For laymen description of
these same herbs, please refer to
Twelve
Important Herbs to Know )
The following list represents the most well-researched herbs
for stroke prevention:
Garlic Allium sativa
Garlic is one of the most important cardiovascular botanicals
and best documented blood-thinning agents. It protects
against collagen-induced, arachidonic acid-induced, ADP-induced,
and epinephrine-induced platelet aggregation. Garlic inhibits
cyclooxygenase and lipooxygenase-induced thromboxane A2 synthesis.
Clinical studies have also documented garlic’s effectiveness in
treating many factors involved in atherosclerosis, including high
blood pressure, high LDL-cholesterol, and high triglycerides.
Garlic decreases platelet aggregation while simultaneously
increasing HDL cholesterol and fibrinolysis.
Ginkgo Ginkgo biloba
Ginkgo exerts considerable effect on platelet aggregation,
adhesion and degranulation. Specifically, ginkgo inhibits platelet
activating factor (PAF) and reduces platelet aggregation induced
by ADP, collagen, and arachidonic acid. It has
membrane-stabilizing, antioxidant and free radical scavenging
effects, and improves blood flow, oxygen and glucose utilization
in the brain. Ginkgo biloba extract (GBE) stimulates
endothelium-derived relaxing factor (EDRF) and prostacycline.
In animal studies, GBE has shown to stimulate nerve cell
regeneration, making it potentially useful both for stroke
prevention and post-stroke treatment.
Turmeric Curcuma longa
Curcumin, the yellow pigment of Curcuma longa, has potent
anti-inflammatory and antioxidant effects. It inhibits platelet
aggregation by inhibiting thromboxanes and leukotrienes and
promoting the formation of prostacycline.
Bromelain Anasas comosus
Bromelain is a mixture of enzymes found primarily in the stem
of the pineapple plant. It exerts antiinflammatory effects by
inhibition of pro-inflammatory prostaglandins. Bromelain blocks
production of kinnins and possesses fibrinolytic activity
secondary to plasminogen activator, which may also account for the
anti-metastatic properties seen in vivo.
Bilberry Vaccinium myrtillus
The flavonoids in Bilberry, specifically anthocyanosides,
promote prostacycline production and inhibit platelet aggregation
in a manner similar to ginkgo. The potent antioxidant effects seen
in this herb stabilize the vascular system and are therefore
useful in treating capillary fragility, venous insufficiency, and
varicose veins.
Grape Seed Vitus vinifera
Oligomeric proanthocyanidin complexes (OPC’s) from grape seed
and other species, such as Landis’ pine, is one of the most potent
antioxidants known. OPC’s trap reactive oxygen species including
hydroxyl radicals, peroxyl radicals, and lipid radicals; they also
delay the breakdown phase of lipid peroxidation. OPC’s inhibit
platelet aggregation in part by raising cGMP levels and protecting
against epinephrine renewed cyclic flow reductions. In addition,
OPC’s inhibit certain proteolytic enzymes, including collagenase,
elastase, beta-glucuronidase and hyaluronidase which can damage
the extracellular matrix surrounding capillary walls. This makes
OPC’s a useful choice for improving vascular fragility and
peripheral vascular insufficiency which can lead to
thrombophlebitis.
|
