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What Is?
What is Stroke
How to Treat Stroke
Natural Treatments for Stroke

What is cardiovascular disease?

Cardiovascular disease (CVD) is the general term for blood vessel disease of the heart or body. CVD is the most common disease process in Western society and the financially well-off sections of developing countries. Blood vessel disease, called atherosclerosis, is the build up of atheroma or plaques along arterial walls, which leads to narrowing or complete blockage of the artery. Significant narrowing reduces the amount of arterial blood to an organ or body region, causing tissue hypoxia, reduced cell metabolism, and organ dysfunction.

In Australia, CVD is a very common and serious disease with about 3.5 million people reporting having the condition in 2007-08. Even though diagnosis, prevention, and treatment methods have improved considerably of late, CVD remains the cause of more deaths than any other disease – about 50,000 in 2008. CVD cost the health budget about $5.9 billion in 2004-05, making it Australia’s most expensive disease.

In Australia, people in lower socioeconomic groups, Aboriginal and Torres Strait Islander people, and people living in remote locations, are more likely to be affected by CVD compared with the rest of the population.

There are four main types of CVD, which cause ischaemia or a lack of blood flow.

  • Ischaemic heart disease of coronary artery disease can cause a myocardial infarction or heart attack.
  • Cerebrovascular disease (of the brain) can cause a stroke or cerebral infarct.
  • Peripheral artery disease of the arms and legs can cause claudication (calf pain with walking), distal tissue atrophy, and in severe cases gangrene.
  • Renovascular disease affects blood flow to the kidneys and can cause renal failure.

If a blood clot forms over the atheroma, this can break off and block smaller vessels downstream. Doctors call this problem arterial thrombosis. Depending on the artery affected than can cause a heart attack, a stroke, or gangrene of a limb, foot or hand.

Cardiovascular disease facts and trends in Australia

Cardiovascular disease facts and trends in Australia

Based on self-reports from the 2007–08 National Health Survey, an estimated 3.4 million Australians (17% of the population) had one or more long-term cardiovascular diseases (CVD).

  • Nearly 50,000 deaths were attributed to CVD in Australia in 2008 – more than any other disease group and 34% of the total.
  • CVD was the main cause for 475,000 hospitalisations in 2007–08 and played a secondary role in a further 797,000.
  • CVD accounted for about 18% of the overall burden of disease in Australia in 2003, with coronary heart disease and stroke contributing more than 80% of this burden.
  • CVD remains the most expensive disease group in Australia, costing approximately $5.9 billion in 2004–05. Just over half of this money was from the cost of admitting patients to hospital for treatment.

The overall death rate for CVD has fallen by about 80% since the 1960s and continues to fall. Death rates from coronary heart disease, stroke, heart failure, rheumatic heart disease, and peripheral vascular disease, have all fallen markedly during the past 20 years. (Cardiovascular disease – Australian Facts 2011)

What is cerebrovascular disease or stroke?

What is cerebrovascular disease or stroke?

When a person has a stroke, the blood flood to the brain has been affected either by a blocked blood vessel or because an artery ruptures causing localised bleeding, called a haemorrhage. Two types of stroke can occur but an ischemic stroke is the most common. When an artery that supplies the brain with blood gets blocked brain cells die because the area is deprived of oxygenated blood. The extent and location vary greatly, as do the resultant symptoms.

A haemorrhagic stroke occurs when one of the arteries in the brain ruptures, usually because of uncontrolled hypertension. The resultant haemorrhage, or localised bleed, affects brain function. An intracerebral haemorrhage is a bleed within the brain tissue and a subarachnoid haemorrhage is a bleed in to the space around the brain.

Short, recurrent episodes of cerebrovascular ischaemia, called Transient Ischaemic Attacks (TIAs), often precede a major stroke and act as a warning sign. TIAs occur before approxi¬mately 50% of cases and present as sudden onset but short-term, temporary symptoms such as dizziness, confusion and disorientation, visual disturbance or loss of vision, skin tingling or loss of feeling, muscle weakness or even paralysis.

TIAs may also occur during an episode of migraine headache, due to arterial vascular spasm. The incidence of stroke is increased in patients with a history of frequent and prolonged episodes of migraine headaches.

Ischaemic heart disease is the most common cause of death among Australians. Cerebrovascular disease, or stroke, is the second most common cause of death and the leading cause of disability for adult Australians. During 2011, 11,251 people Australians died from stroke.

According to the Australian Institute of Health, in Australia during the period 2009–10, 0.4% of patients (35,345) who were admitted to hospital for treatment had suffered a stroke. Among people hospitalised for treatment of cardiovascular disease, 7% had suffered a stroke.

Signs and symptom of a stoke

Signs and symptoms of a stoke

A stroke in an emergency situation and only a doctor or paramedic can decide whether a stroke has occurred A stroke occurs when blood supply to the brain is interrupted. When an artery becomes blocked or ruptured, that part of the brain is deprived of oxygenated blood and important nutrients and dies. Facial weakness, arm weakness and difficulty with speech are the most common symptoms of stroke.

Assume that a person has had a stroke if any of these FAST symptoms are observed:
Face – one side of the face droops
Arm – unable to lift one or both arms in the air
Speech – unable to speak or speech is slurred or jumbled
Time – urgent treatment is important

Some treatments can only be given by a doctor, and must be administered with three (3) hours of the stroke starting. If you think a person is having a stroke call triple zero (000) and ask for an ambulance.

Neurologic complaints vary from focal motor or sensory disturbances and speech defects to profound coma and including:

  • Premonitory symptoms may include headache, dizziness, drowsiness, and mental confusion
  • Specific derangements of speech, thought, motion, motor function, sensation or vision usually occur,
  • Focal signs and symptoms are usually associated with blockage of particular arteries

A person having a stroke can experience multiple symptoms on sudden onset. In the conscious patient, substantial confusion and disorientation are usually present, often associated with headache, vomiting and convulsions, a stiff neck, and abnormal muscle reflexes.

Other signs and symptoms of a stroke

Other signs and symptoms of a stroke

  • Weakness or numbness or paralysis of the face, arm or leg
  • Difficulty speaking or understanding
  • Dizziness, loss of balance, or unexplained fall
  • Loss of vision, sudden blurring, or decreased vision
  • Headache, usually severe and abrupt
  • Unexplained change in the pattern of headaches
  • Difficulty swallowing

Some strokes are preceded by mini or temporary strokes called transient ischaemic attacks (TIAs). If the signs of stroke are intermittent and resolve with hours or the next day, the person might be having a TIA, which are a precursor to more severe stroke. A patient displaying the signs of TIA requires a thorough medical assessment to prevent a debilitating stroke.

How is a stroke diagnosed?

How is a stroke diagnosed?

A person suspected of having cardiovascular disease (CVD) needs a thorough assessment by their doctor. This will involve questions about medical and family history, and lifestyle risk factors. Often a blood test is arranged to determine cholesterol and lipid levels.

A brain CT or MRI will show whether a person has had a stroke, which area of the brain has been affected, and how much of the brain has been affected. Other areas might need to be examined if an arterial embolus is suspected, to prevent further problems. Atheromatous plaque in the neck (carotid) arteries or heart may have broken off and lodged in a brain artery. Surgical treatment of the embolic source may be necessary.

If symptoms are convincing, further tests may be needed to assess the extent of CVD, such as an ECG, angiography, Doppler ultrasound, or stress echocardiography, depending on the region affected.

What are the risk factors for a stroke?

What are the risk factors for a stroke?

Cardiovascular disease (CVD) is the general term for arterial disease of the heart, brain, and body. Stroke is when the brain affected by arterial blockage or haemorrhage into the brain. The risk factors for CVD and stroke are therefore very similar.

Stroke risk factors that cannot be changed are age, gender, and family history of stroke. Medical stroke risk factors include TIAs, atrial fibrillation, Type 2 diabetes, and fibromuscular dysplasia.
Lifestyle-related risk factors that can be modified include high blood pressure, high cholesterol, cigarette smoking, excess weight and obesity, excess alcohol, poor diet, and lack of exercise.
Elderly people are at increased risk for stroke. People aged 85 years and over have almost twice the risk for stroke compared with the 75–84 year age group, and 11 times the rate among those aged 55 to 64 years.
Approximately 65% of hospitalisations to treat stroke occurred in people aged 70 years and over. Men show a higher incidence of CVD, which is also reflected in stroke hospitalisation rates.
A person with atrial fibrillation is five times more likely to suffer a stroke and approximately 15% of stroke patients have atrial fibrillation – when the two upper heart chambers (atria) beat rapidly and unpredictably. The lack of proper contraction can lead to an atrial blood clot, which can travel to the brain to block oxygenated blood and nutrients reaching the brain. This type of stroke is called an embolic stroke or cardio-embolic stroke.
Unfortunately, many people with atrial fibrillation are unaware they have the problem. Signs of atrial fibrillation include heart palpitations, a sudden pounding or racing sensation in the chest, and feeling light-headed. A simple pulse check at the wrist or neck will demonstrate whether a heartbeat is irregular.
In developed countries, the most common cause of stroke is arterial disease of the brain or heart arteries, high blood pressure, diabetes and high levels of homocystine in the blood.

In developing countries, severe dehydration secondary to gastroenteric infection and cerebral trauma contribute to stroke. Myocardial and vascular infections, such as endocarditis, rheumatic fever and vasculitis, and tertiary syphilis are more common in developing countries.

What are some related conditions?

What are some related conditions?

Blood pressure (BP) is a measurement of the force of blood as it travels through the arteries of the body. An arm cuff (sphygmomanometer) with an internal balloon is inflated over the upper arm artery, to intentionally block blood flow. Deflating the cuff will allow blood flow to return in two phases that correspond to the heartbeat – systolic pressure and diastolic pressure.

High blood pressure means the blood pressure measurement are higher than what cardiologists have determined is the normal range.

The National Heart Foundation of Australia defines normal adult BP as < 120/80 mmHg. Normal BP range is between 120/80 and 140/90 mmHg. High BP is 140/90 mmHg or higher. [/su_spoiler] [su_spoiler title="How can a stroke be prevented" style="fancy"]

How can a stroke be prevented

The most effective way to prevent cardiovascular disease (CVD) is to modify risk factors. While some risk factors such and age, race, and gender are fixed. Behaviour and biomedical risk factors can be changed to reduce an individual’s risk of developing CVD.

The build up of atheromatous plaque in an artery that leads to CVD is largely preventable. By stopping cigarette smoking, choosing nutritious foods, lowering salt in the diet, exercising, keeping weight down, and drinking less alcohol, a person can reduce his or her risk of developing CVD. If you’re more than 50 years of age, ask you medical doctor to assess your risk for CVD.

Low to moderate alcohol consumption can protect a person against hypertension, ischaemic heart disease, stroke, and gallstones for some subgroups of the population. The cardiovascular health benefit of low to moderate alcohol consumption relates mainly to men over 40 years of age and post-menopausal women.

However, don’t over indulge. For healthy men and women, drinking no more than two standard drinks on any day reduces your risk of harm from alcohol-related disease or injury over a lifetime. MORE>

Glossary – Stroke terms


Alpha-linolenic acid – an essential omega-3 fatty acid and organic compound found in seeds, nuts, and many common vegetable oils
Aneurysm – balloon dilatation of an artery due to atherosclerosis
Ascorbic acid –¬ vitamin C
Aspirin – a salicylate drug used to treat pain, fever, arthritis, and inflammation, and reduce the risk of heart attack
Arteriosclerosis (athersclerosis) – disease of wall of arteries, also called hardening of the arteries
Atheroma – accumulation of degenerative plaque along the inner artery wall
Atrial fibrillation – abnormal heartbeat due to rapid, irregular contraction of the upper heart chambers called the atria
Bowel dysbiosis – microbal imbalance of the gut flora (bacteria) usually due to repeated antibiotic use
Cerebrovasular disease – disease of the arterial vessels that supply the brain
Cardiovascular disease – disease of the arterial vessels that supply the heart.
Cholesterol – a lipid compound needed to build and maintain membranes present in dietary animal fats. High cholesterol levels is a risk factor for cardiovascular disease.
Claudication – leg cramping and pain during exercise, due to lack of blood supply to the legs
Cardiomyopathy – weakening of the heart muscles causing heart failure due to inefficient pumping of blood from the heart
Coenzyme Q10 – a dietary suppliment similar to a vitamin needed for cell growth and maintenance
DHEA (dehydroepiandrosterone) – a precursor to sex hormones produced by the adrenal glands
Dipyridamole – a platelet aggregation inhibitor that prevents blood clots from forming
Dyslipidaemia – abnormally high lips levels (fat and choesterol) in the blood
EPA (eicosapentaenoic acid) – a long-chain omega-3 fatty acid (good fat) found in fish and shell fish that provides health benefits
DHA (docosahexaenoic acid) – a long-chain omega-3 fatty acid (good fat) found in fish and shell fish that provides health benefits health benefits
Fibromuscular disease – rare arterial wall disease that can cause arterial narrowing
Flavonoids (bioflavonoids) – a phytochemical compounds synthesised by fruit and vegetables that have antioxidant health benefits
Folic acid – a vitamin B that helps the body make new cells
Glutathione – an antioxidant found in plants that prevents cellular damage
Haemorrhagic stroke – cerebral infarct due to small vessel rupture in the brain
HDL cholesterol – a ‘good’ lipoprotein cholesterol that appears to removes excess cholesterol. HDL levels below 40 mg/dL are considered too low.
Hemiplegia – unilateral (one-sided) paralysis of the body or part of the body associated with stroke
Hepatic detoxification – one of the liver functions is to detoxify the blood stream
Hexaniacinate – a form of vitamin B3 that coverts the energy content of food to aid the function of the skin, nerves and digestive system
Hypertension – high blood pressure
Hypoxia – inadequate supply of oxygenated blood
Ischaemic stroke – brain cell death due to inadequate blood supply
LDL cholesterol – a ‘bad’ lipoprotein cholesterol associated with an increased risk of cardiovascular disease. Ideally LDL levels should be <160 mg/dL Lipoic acid – organosulfur compound antioxidant and a cofactor for enzyme systems N-acetyl-cysteine – nutritional supplement antioxidant and liver protectant NADH – a coenzyme supplement that can improve energy levels and protects the liver from alcohol damage Pantethine – a form of vitamin B5 that supports lipid metabolism Polycatechins – green tea extract and chemoprotective agent for cancer Polycosanol – decreases cholesterol production in the liver and improves breakdown of LDL cholesterol Sphygmomanometer – device used to measure blood pressure Stent – a synthetic tube used to open a blocked arter Thrombolysis, also known as thrombolytic therapy, is a treatment to dissolve dangerous clots in an artery or vein, improve blood flow, and prevent ischaemic damage to tissues and organs. Thrombolytic agent – a drug injected into an artery or vein to break up an occlusive blood clot Tocopherols – vitamin E an antioxidant that helps protect the structure of cells and enhances the proper function of nerves and muscles Transischaemic attack – short-term episodes of blood deprivation to the brain. Identical symptoms to stroke symptoms but the symptoms resolve within minutes to hours. [/su_spoiler] [/su_accordion]

Conventional medical treatments doctors use to treat stroke

When a person has a debilitating stroke it can change his or her life forever. Australian hospitals now have specialist Stroke Care Units that can provide thrombolysis treatment with a drug such as alpetase, to dissolve brain clots, if the patient arrives within three hours of the stroke starting. List of Australian hospitals with stroke care units. Because these drugs have dangerous side effects, strict guidelines are in place to determine the appropriate circumstances for use. MORE>

The most appropriate treatment will depend on the type of stroke and the cause. Anticoagulant drugs, which thin the blood, may be prescribed to prevent new blood clots forming and to prevent a second stroke. Examples of blood thinning medications are aspirin, aspirin plus dipyridamole (Asasantin), clopidogrel (Plavix) and warfarin (Coumadin or Marevan).

Thrombolysis is usually successful in 75% of cases, but the treatment is not able to dissolve the blood clot in up to 25% of patients. Although blood flow is restored as a result of the treatment, 12% of patients subsequently redevelop the clot or blockage in the blood vessel, during the weeks or months following treatment.

If the cause of stroke is a narrowed or blocked carotid artery in the neck, a vascular surgeon may need to surgically remove the atheromatous plaque that caused the arterial embolus or ischaemia. This operation is called a carotid endarterectomy.

Rehabilitation after a stroke

Rehabilitation after a stroke

Whether a stroke patient can fully return to previous activities will depend on the extent and location of brain damage. Recent advances in rehabilitation enable many people who have had a stroke to return to active lives. However for many, recovery can take many months, even years to achieve. The age of the patient will affect the effectiveness of rehabilitation. Older patients do not recover as well as younger patients.

Family support plays an important role in rehabilitation, by having conversations to regain speech, and much needed encouragement and motivation to perform daily tasks.

Therapy involves respective practice using the affected muscles, including:

  • Physiotherapy to improve muscle control, co-ordination and balance
  • Speech therapy to retrain facial muscles and language
  • Therapy to overcome feeding and swallowing disorders, and
  • Occupational therapy to improve hand–eye co-ordination and skills needed for daily living tasks.

If a person has stroke symptoms, call triple zero (000) immediately and ask for an ambulance.

During a stroke, every minute counts and knowing the FAST assessment for signs and symptoms could save a life. Assume that a person has had a stroke if any of these symptoms are observed:
Face – one side of the face droops
Arm – unable to lift one or both arms in the air
Speech – unable to speak or speech is slurred or jumbled
Time – urgent treatment is important

Nutritional medicine treatment after a stroke

The immediate and medium-term treatment goals are to salvage brain function and restore the patency of vessels.

Once brain tissue dies it can’t be salvaged. However, some brain tissue adjacent to the problem area might be salvageable using high dose antioxidants such as vitamins C and vitamin E and glutathione, plus other nutrients such as magnesium, taurine, adenosine and acetylcarnitine.

These nutrients can limit the size of the area that dies, and restore brain function, when administered intravenously after an ischaemic stroke.

Short-term treatment by nutritional medicine focuses on reducing platelet aggregation and stabilising the wall of the artery, after an ischaemic stroke.

In the medium- and long-term, anti-platelet medication, such as aspirin and clopidrogel, is beneficial, with several studies reporting that these agents reduce the risk of further stroke by about 30-40%.

However, there is doubt about whether or not this form of therapy alters long-term survival, with contemporary evidence suggesting no long-term advantage accrues. An increased risk of haemorrhagic stroke and gastric haemorrhage in patients on long-term therapy has been documented.

Stabilisation and partial restoration of areterial flow may be achieved by utilising the platelet anti-aggregation effect of vitamin E and omega-3-fatty acids, with additional vitamin C and flavonoid compounds such as quercetin. Two phytonutrient extracts that may also aid recovery are gingko biloba and coleus forskolii, which can reduce platelet aggregation, improve cerebral circulation, and reduce blood pressure.

The advantage of a nutrient-based therapy is that, while reducing platelet aggregation, it also promotes normalisation of vascular endothelial function and enhances tissue antioxidant capacity, with a much reduced risk of causing accidental haemorrhage.

The goals of nutritional medicine treatment of stroke are to restore brain function, reduce platelet aggregation, and stabilise the arterial wall to prevent further stroke events.

Long-term treatment of stroke

Long-term treatment of stroke

Long-term therapy should be focused on improving vascular patency and circulatory competence, while enhancing compensatory retraining of other brain areas.
Brain tissue is ‘plastic’ and can develop new functional networks that may compensate for those damaged as a result of the stroke event.

Evidence from clinical work suggests that a substantial degree of neuronal regeneration and improved brain plasticity may be achieved using nutrients, such as acetyl-carnosine, alpha-lipoic acid and S-adenosyl-methionine, in combination with nootropic agents, such as hydergine, pira¬cetam, centrophenoxine and nicotinate derivatives, optimised diet, antioxidant therapy, and coordinated physical rehabilitation.

Because of the debilitating effects of stroke, optimal treatment of cerebrovascular disease hinges on prevention. Identifying and correcting nutritional and functional disturbances that are known to contribute to vascular disease could prevent future episodes. The nutritional medicine practitioner will focus on identifying and correcting the known causes of cerebrovascular disease, including:

  • Insulin resistance
  • Hypertension
  • Dyslipidaemia
  • Platelet aggregation activity
  • Vascular endothelial integrity
  • Brain tissue antioxidant capacity
  • Essential fatty acid metabolism and balance, and
  • Neuronal homocysteine metabolism.
What is insulin resistance?

What is insulin resistance?

A consequence of genetic influence and lifetime dietary intake, insulin resistance is a major causal factor in the development of arterio¬sclerosis and hypertension, the major predisposing factors to cerebro¬vascular disease and stroke.

A person with untreated insulin resistance could progress to Type 2 diabetes, which has a fourfold increase in the incidence of stroke and heart attack. Early detection and pro-active dietary and nutritional therapy is important in preventing stroke.

However, diet prescription is currently a very contentious issue in nutritional therapy of insulin resistance and vascular disease.

The more orthodox recommendation is a strict low-fat, high-fibre diet, with high-carbohydrate but low-GI foods making up 60-70% of food. However, recent studies have raised concerns that such a diet induces a substantial degree of lean-weight loss while having only modest impact on insulin production and dyslipidaemia – two major factors in the development of vascular disease. Such a diet might contribute unwittingly to making insulin resistance worse.

The Mediterranean-style diet is based on a high intake of olive oil, vegetables, and low-GI pasta and bread, along with a reasonable amount of lean meat and seafood.

The Mediterranean diet is shown to correct insulin sensitivity, and lower bodyweight and blood lipids. However, whether this diet can lower food-induced insulin production in people with a strong genetic tendency towards pancreatic B-cell hyper-responsivity and hyperinsulinaemia, as occurs in Sardinia and Sicily, remains unproven.

Most controversial of all is the low-carbohydrate and high-protein diet, in which carbohydrates are markedly restricted, in particular those that are refined or simple sugars or are high GI.

Recent studies indicate that this form of diet, despite its obviously high saturated fat intake, does result in a markedly reduced insulin response to meals, reduces upper abdominal fat and reduces overall weight, while maintaining lean-weight. The Mediteranian diet helps keep triglyceride and HDL cholesterol at ideal levels, and corrects high lipid levels in the blood.

Important to any diet is a high proportion of a wide variety of fresh fruit and vegetables. Research show that including high-fibre flavonoid-rich foods reduces cardiovascular disease and Type 2 diabetes.

The optimal diet depends on the degree of insulin resistance and so a diet to optimise insulin efficiency needs to be customised to a person’s individual metabolic and social lifestyle. A nutritional specialist will monitor the effects using indices of insulin resistance and alter the diet accordingly.

All dietary recommendations can be modified, in line with patient response.

Controlling hypertension is key to preventing a stroke

Controlling hypertension is key to preventing a stroke

Optimal control of hypertension is a prerequisite to successful treatment and prevention of stroke. This can be achieved through maximum attention to appropriate diet and regular exercise, particularly with respect to improving insulin resistance, and the judicious use of phyto¬nutrient extracts (crataegus, gingko, garlic) and/or medications (ACE inhibitors).

Salt restriction is usually promoted as a major nutritional control mechanism for hypertension and may certainly be effective in salt-sensitive patients, who exhibit a fall in mean arterial blood pressure (BP) when they consume a low-salt diet and a rise in mean arterial BP when they consume a high-salt diet. In these patients, shifting salt consumption across to a mineral salt containing a mix of sodium, potassium and magnesium may be more beneficial than simply attempting to minimise salt intake.

Contemporary studies into the biological role of nitric oxide (NO) indicate that vascular endothelium NO production is essential to maintenance of endothelial integrity and arterial muscle tone.

Reduced NO production has been identified as a major causal factor in the development of hypertension and appears to be causally related to elevated free fatty levels, insulin resistance and increased superoxide and lipid peroxidation products in the vascular tree.

Improved NO production induced by diet and antioxidant therapy, such as ascorbate and vitamin E, is reported to substantially reduce blood pressure to a greater extent than does salt restriction.

Controlling dyslipidaemia (abnormal level of lipids) to prevent stroke

Controlling dyslipidaemia (abnormal level of lipids) to prevent stroke

Proactive control of dyslipidaemia is reported to substantially reduce the risk of cerebrovascular disease and stroke and medically may be achieved by HMG-CoA Reductase inhibitory drugs – the ‘statin’ drugs.

These lipid-lowering agents have been shown to also improve peripheral glucose disposal, thus reducing insulin resistance, and enhance vascular endothelial function, thereby retarding the development of both small and larger artery disease. However, they do carry significant risk of adverse effects by interfering with synthesis of cholesterol, cholesterol-derived steroid hormones and cellular production of ubiquinone (coenzyme Q10).

Recent studies also suggest these drugs appear to increase insulin resistance and reduce tissue antioxidant status. Thus, alternative therapeutic strategies may be preferable to statin therapy and are reported to confer equal benefit with reduced adverse effects, improving patient blood lipid profiles and health status, and reducing mortality rates and morbidity.

Reducing platelet aggregation activity to prevent stroke

A major risk for stroke is platelet activation, which increases the tendency to thrombosis that may occur in a peripheral, coronary or cerebral artery. This risk is mag¬nified in arteries with arteriosclerosis plaques, where plaque rupture or ulceration exposes blood borne platelets to denatured collagen and other pro-aggregatory metabolites, causing local thrombosis.

The potential for platelet activation is dependent on the balance between platelet thrombox¬ane (TXA-2) production, derived from arachidonic acid, and production of anti-aggregatory prostanoids, derived from DHGLA and EPA.

As thrombosis is thought to be the main cause of an acute ischaemic event, prevention of myocardial infarction and stroke centres on the use of aspirin and clopido¬grel, which inhibit platelet activation and reduce thrombosis risk.

Current evidence with stroke-risk patients indicates that this therapy is beneficial only in those with a very high risk, whereas in those with a low-medium risk, the potential for a serious haemorrhagic event outweighs the benefit of treatment. Also, the use of clopidogrel shows no extra benefit than use of the more economical, low-dose aspirin.

Anti-platelet effects equivalent to aspirin may also be achieved using natural agents, usually in combination, such as vitamin E and omega-3-fatty acids, flavones and bioflavonoids, and the phytonutrients garlic, gingko biloba and coleus. These natural agents have been reported to reduce platelet TXA2 production and enhance synthesis of favourable prostanoids, as well as stabilising the platelet membrane and reducing the activation potential.

However, though the risk of haemorrhagic events with natural therapy is less than that for aspirin or clopidogrel, a slight increase in stroke has been reported following aggressive use of fish-oil and gingko biloba, therefore patients still require close monitoring of platelet aggregation and bleeding time and appropriate reduction in therapeutic dosage if indicated.

Improving vascular endothelial integrity

Improving vascular endothelial integrity

Over recent years, it has become apparent that endothelial function is an active process, whereby endothelial cells secrete the antithrombotic prostaglandin, prostacyclin, aka PGE-1, derived from arachidonic acid. Similar prostanoids derived from DHGLA and EPA also exhibit equivalent activity, and therapeutic use of these agents confers the added benefit of reducing platelet TXA2 synthesis and the platelet pro-aggregatory potential.

Vascular endothelial cell prostacyclin synthesis is apparently mediated via nitric oxide (NO) production by endothelial cell NO-synthetase (NOS). NO synthetase occurs as a non-inducible form – NOS-1 – that maintains a relatively constant low-level activity, and inducible forms, e-NOS and NOS-2, whose activity varies with prevailing internal stimuli, such as bacterial LPS exposure, chemical toxins, free fatty acid concentration, cytokine levels, and tissue antioxidant capacity.

While endothelium-derived NO production is essential to the maintenance of endothelial integrity and control of tissue vasodilation and platelet aggregation, excessive NO production contributes to increased endothelial oxidative damage that promotes LDL-cholesterol oxidation, and enhanced macrophage activation and BBB permeability. Increased cerebral NO production, triggered by ischaemia and release of Platelet Activating Factor (PAF) and Tumour Necrosis Factor-alpha (TNF-a), causes NMDA receptor activation and progressive neuronal damage, which is further augmented by elevated lipid-derived prostanoids and depletion of cerebral tissue GTH levels.

Conversely, impaired endothelium NO production is reportedly linked to elevated blood fatty acid levels and lipid peroxidation products and is apparently causally involved in the development of hypertension and insulin resistance. In these patients, supplemental ascorbate, mixed tocopherols and arginine is reported to increase NO production and vascular dilation, promoting improved glucose dispersal and reduction in hypertension.

Brain tissue antioxidant capacity

Brain tissue antioxidant capacity

Brain tissue antioxidant capacity plays a vital role in protecting neurones from oxidative damage and the weight of evidence indicates that chronic antioxidant insufficiency is implicated in progressive neuronal damage in both acute and chronic ischaemic conditions.

While brain tissue has a high demand for oxidative processes and a corresponding high demand for antioxidant protection, it lacks glutathione synthetase activity. The brain is therefore dependent on the absorption of glutathione, derived mainly from hepatic GTH production, to maintain adequate tissue GTH activity.

Under acute demand conditions or because of impaired hepatic production, brain GTH levels may become inadequate to demand, leading to oxidative damage and neuronal death. A further factor that contributes to this propensity to oxidative damage is the limited transport of ascorbate across the BBB, such that brain tissue ascorbate levels may run well below blood levels, particularly in times of acute antioxidant demand.

Essential fatty acid metabolism and balance

Essential fatty acid metabolism and balance

The majority of arachidonic acid (an Omega-6-FA metabolite) and docosahexaenoic acid (an Omega-3-FA metabolite) is sequestered into the brain tissue cell membranes and the relative balance between these two essential fatty acid metabolites governs local tissue production of cytokines and inflammatory mediators such as PAF and TNF-a, as well as neuronal membrane integrity and neurotransmitter receptor activity.

Inadequate Omega-3-FA absorption enhances inflammatory mediator responses, while inadequate Omega-6-FA appears to reduce neuronal membrane stability leading to impaired responsivity and symptoms of ‘central’ fatigue, as occurs also in Chronic Fatigue Syndrome.

>h2>Improving Neuronal homocysteine metabolism

Neuronal homocysteine metabolism is dependent on adequate brain tissue levels of vitamins B12 and B6, folic acid, and betaine (derived from trimethylglycine). A reduced tissue level of these nutrients is associated with increased neurotoxicity related to increasing tissue homocysteine concentration.

Unfortunately, with advancing age and impaired blood-brain-barrier permeability, brain levels of these nutrients may fall well below blood levels, leading to progressive neuronal damage and impaired brain function.

Contemporary studies report that excessive nitrous oxide production within neurones inhibits the vitamin B12 dependent metabolic pathway, whereby homocysteine is converted back to methionine, causing a functional B12 insufficiency that leads to impaired neuronal function and increased risk of degenerative disease and cerebral arteriosclerosis. Supplemental B12, B6 and folic acid are reported to reduce homocysteine levels and retard development of degenerative neurological and cerebrovascular disease.

Nutritional medicine treatment for stroke - summary

Nutritional medicine treatment for stroke – summary

Assess individual patient requirements:

  • Determine the presence of insulin resistance, Syndrome X, hypertension and other evidence of vascular disease
  • Assess insulin levels before and after carbohydrate consumption and check HbA1c level
  • Measure blood lipid levels plus serum levels of Lp(a), Apolipoprotein B and homo¬cysteine
  • Measure platelet aggregation activity, ESR and CRP and possibly red cell membrane EFA composition
  • Check APO-E genotype
  • Test total antioxidant capacity and GTH levels if possible – possibly also ascorbate and tocopherol levels
  • Measure body composition and Type II nutrient status, especially protein, zinc, magnesium status
  • Check for bowel dysbiosis, increased cytokine production and food reactivity, especially antigliadin antibody levels
  • Assess hepatic detoxification capacity
  • Measure hormonal status, particularly anabolic steroids and IGF-1

Dietary prescription: according to individual assessment findings but bear in mind that cerebrovascular risk is reduced by the following manipulations:

  • Increase fruit and vegetables – thereby increasing dietary intake of flavonoids, antioxidants, essential minerals and fibre and reducing high GI carbohydrate intake.
  • Increase fish and meat protein intake. Vegetable proteins derived from soybean and other legumes, but not cereals, is associated with increased stroke risk, though the causal mechanism has not yet been defined.
  • Maintain animal protein and lipid intake at adequate levels and particularly maintain cholesterol at a moderate level
  • Increase monounsaturated and omega-3-fatty acid intake – note that milk-derived fats appear to be protective
  • Reduce salt intake or shift to a mixed mineral salt with potassium and magnesium – only implement severe salt restriction if patient is highly sensitive
  • Alcohol – maintain low-level alcohol intake – utilise antioxidant benefits of red wine but restrict beer intake because of its high GI
  • Low-allergy diet is required if testing reveals food allergy or sensitivity reactions are present, in particular check gluten and milk protein reactions

Nutrient supplementation: according to individual requirements as determined by nutritional assessment but need to bear in mind the reported benefits of the following nutrients:

  • Digestive enzyme therapy, particularly if bowel symptoms and/or Type II nutrient insufficiency is present
  • Antioxidant supplements: ascorbate, mixed tocopherols, flavonoids and polycatechins,
  • Antioxidant metabolites: coenzyme Q10, lipoic acid and N-acetyl-cysteine
  • Omega-3-EFA supplements: alpha-linolenic acid, EPA and DHA
  • Nutrients to reduce high cholesterol levels: hexaniacinate, pantethine, polycosanol, red yeast rice
  • Nutrients to control homocysteine levels: folic acid, betaine, vitamin B6 and vitamin B12 and possibly vitamin C
  • Essential minerals: particularly magnesium, potassium and zinc
  • Therapeutic supplements to correct bowel dysbiosis and hepatic detoxification problems if present