Parkinson's disease (paralysis agitans, shaking palsy) was first described in 1817. It is now increasingly clear not only what causes Parkinson's, but also how it can be prevented and its relentless progress slowed down.
Environmental and Dietary Factors. Parkinson-like symptoms can occur as a result of head injuries, carbon monoxide poisoning or poisoning by pharmaceutical or other drugs. Certain diuretics (reserpine), antipsychotics (chlorpromazine), and heart drugs (verapamil) have all been implicated in causing or worsening Parkinson's disease symptoms as has the "designer drug" MPTP (methylphenyl-tetrahydropyridine). In some cases, drug-induced Parkinson's disease may be halted or reversed if the drug is promptly withdrawn. Naproxen and other NSAIDs may also exacerbate Parkinson's disease.
Recent research carried out in Iceland, which has a very high incidence of Parkinson's disease, has shown that children born during or after a whooping cough (pertussis) epidemic are particularly vulnerable to Parkinson's disease in later life. This finding supports the idea that Parkinson's disease may develop later in life as a result of a neurotoxic event that occurred at an early age.
The main pathological feature of Parkinson's disease is the progressive destruction of dopamine-producing cells in the substantia nigra region of the brain stem. The loss of dopamine production affects the balance between dopamine and acetylcholine in the brain with the result that messages to the muscles become garbled. It is estimated that the characteristic Parkinson's disease symptoms develop once 70% of the dopaminergic neurons in the substantia nigra have been destroyed.
Until recently there were few alternative treatments available for Parkinson's disease patients. This is now changing. The finding that Parkinson's disease is almost certainly caused by oxidative stress aggravated by metal toxicity is a major step forward in understanding and eventually conquering the disease.
The fact that antioxidants retard the development and slow the progression of existing Parkinson's disease was demonstrated in 1991 in a pilot study carried out by Dr. Stanley Fahn of Columbia University. The overall conclusion of this research is that one can lower one's risk of developing Parkinson's disease by reducing one's intake of animal fats and sugar, avoiding excessive exposure to metals such as aluminum, iron, manganese, mercury, cadmium and copper, and by ensuring an adequate intake of antioxidants. These preventive measures may also be useful in slowing down the progression of the disease.
Symptoms of Parkinson's disease include stiffness or slowness of movement, a shuffling walk, stooped posture, and difficulties in performing simple tasks.
Those suffering from Parkinson's disease often have difficulty in performing simple tasks.
About half of all Parkinson's Disease sufferers have difficulty speaking.
Signs of Parkinson's disease include stiffness or slowness of movement, a shuffling walk, stooped posture, and difficulties in performing simple tasks.
A shuffling walk is characteristic of Parkinson's disease.
A study published in 2003 in The Archives of Neurology found that people who rapidly develop symptoms of Parkinson's disease may be up to 8 times as likely to develop Alzheimer's disease. The study found that the physical symptoms of Parkinson's disease are linked to a decline in mental functioning as seen in Alzheimer's disease. About 15% of Parkinson's disease victims eventually develop Alzheimer's disease, and another 15% develop other forms of dementia.
Memory impairment and cognitive dysfunction are rarely encountered in early stage Parkinson's disease. However, about 30% of Parkinson's disease victims eventually develop Alzheimer's disease or other forms of dementia.
Depression is a common feature amongst Parkinson's disease victims. Depression may be difficult to diagnose in patients with Parkinson's because the signs of these two disorders overlap. In addition, patients with atypical Parkinson's more often have depression than patients with classical Parkinson's.
The question as to what causes the destruction of the dopamine-producing cells has puzzled researchers for years but a consensus is now emerging that Parkinson's disease is caused by oxidative stress and metal toxicity. The idea that oxidative stress, i.e. an excess of free radicals in the body, can cause disease was first brought forward in 1983. Numerous studies have shown that Parkinson's disease victims have low levels of natural antioxidants (glutathione and superoxide dismutase) and high levels of iron in the substantia nigra areas of their brains. It is believed that iron helps catalyze the free radical reactions that destroy the dopamine-producing cells.
D-phenylalanine (DPA) may be helpful for some individuals with Parkinson's disease. [Arzneimittelforsch 26: pp.577-9, 1976]
Flavonoids, and in particular the proanthocyanidins (grape seed and pine bark extracts) should also be excellent candidates as Parkinson's disease preventers and retarders. Proanthocyanidins are water-soluble antioxidants that are stronger than vitamin C and which readily cross into the brain fluid. Clinical trials are, however, still required to support this hypothesis.
Australian researchers have found that broad beans (Vicia faba) are an extremely good source of l-dopa and can, in some cases, actually replace l-dopa. A 100gm serving of broad beans (including the pods) provides about 250mg of l-dopa and in addition a significant amount of proanthocyanidins. The broad beans remain effective even if canned or frozen, but should always be consumed whole as the pod has been found to have the highest concentration of l-dopa. Medication dosage may have to be adjusted if broad beans are consumed on a regular basis.
The timing of protein intake can markedly increase the effectiveness of l-dopa and thereby lead to reduced dosage requirements. Researchers now recommend that protein intake be kept as low as possible and that protein be included primarily in the evening meal.
Conventional medical treatment relies heavily on l-dopa (levo-dihydroxy-phenylalanine), a dopamine precursor that can cross the blood-brain barrier and is converted to dopamine in the brain. L-dopa is now rarely used by itself, but rather in combination with carbidopa (Sinemet) or benserazide (Madopar) that protects it from breaking down before it reaches the brain tissue. As l-dopa must compete with other amino acids in crossing both from the gut to the blood stream and from the blood stream to the brain it is usually recommended that it be taken between meals rather than with meals.
Although l-dopa medications can bring significant relief from Parkinson's disease symptoms they become less effective with time. After four or five years of increasing dosages their effect becomes sporadic and unpredictable (the "on-off syndrome") and patients become increasingly helpless and depressed. There is also evidence that the use of l-dopa medications may lead to a deficiency of B-vitamins, especially niacin and vitamin B-6. Most Parkinson's disease experts now recommend that l-dopa therapy be started as late as possible after diagnosis of Parkinson's disease so as to postpone the day when it no longer works and to limit its many serious adverse effects.
Selegiline (Deprenyl, Eldepryl) is another drug used in Parkinson's disease therapy. It works by blocking the breakdown of dopamine in the brain. Recent trials have shown that starting Parkinson's disease patients on selegiline can extend the time period before they need l-dopa by about nine months. Combinations of l-dopa medications and selegiline have also been tried in early stage Parkinson's disease patients, but were found to have no advantage. A recent study concluded that the combination therapy increased mortality by about 50% when compared to Parkinson's disease patients treated with l-dopa medications alone.
Anticholinergenic drugs work by reducing the amount of acetylcholine produced in the brain and thereby redressing the imbalance between dopamine and acetylcholine. They are no longer recommended for older patients as they have serious neuropsychiatric side-effects.
C.A. Hackethal, M.D. has reported excellent success in treating Parkinson's Disease by use of replacement therapy of DHEA. Apparently the bad side-effects of L-Dopa are avoided, and the Parkinsonian victim is restored to appropriate functioning.
Other antioxidants such as coenzyme Q10 (ubiquinone) and proanthocyanidins may be equally or more effective than vitamins C and E. This, however, remains to be proven in clinical trials. Coenzyme Q10 is absorbed into brain fluids and is a very powerful antioxidant.
Stress aggravates Parkinson's disease and relaxation therapy has been found useful in the treatment of the disease. A well thought-out program of rest, exercise and physiotherapy can also significantly ameliorate the symptoms of Parkinson's disease.
In a Russian trial, 60 patients with Parkinsonism of various causes with pronounced tremor were effectively treated with intramuscular doses of vitamin B6. Single doses were as high as 400mg; the total doses were from 3000 to 6000mg. Changes in laboratory findings (EMG, tremorographic and myotonometric) correlated with the clinical picture. Vitamin B6 is recommended irrespective of the cause of the disease and of the patient's age, and can be given either alone or in combination with anti-Parkinsonian drugs aside from DOPA. [Sov Med (7): pp14-9, 1979 (in Russian)]
Supplementation with vitamin C and E markedly slows the progression of the disease in its early stages.
Parkinson's disease patients given large doses of oral vitamin C and synthetic vitamin E supplements (3000mg and 3200 IU daily respectively) delayed the progression of their disease to the point where they needed l-dopa 2.5 years later than a group of patients who were not taking supplements. Later research has shown that synthetic vitamin E in itself does not retard the progression of Parkinson's disease. Thus it is likely that it was vitamin C by itself or its combination with vitamin E that was the active component in Dr. Fahn's experiment. This fits with a later finding that vitamin E, a fat-soluble vitamin, does not readily cross the blood-brain barrier nor does it accumulate in the cerebrospinal fluid that bathes the brain. Vitamin C, on the other hand, while not crossing the blood-brain barrier does enter the cerebrospinal fluid and can be found there in concentrations proportional to dietary intake. Inasmuch as vitamin C is a highly effective antioxidant and is particularly adept in quenching hydroxyl radicals (the main culprits in the dopamine-cell destruction), it is becoming increasingly clear that this vitamin may be an excellent protector against Parkinson's disease and can materially help in slowing down the progression of the disease.
Supplementation with vitamin B-complex may be necessary, especially for patients who take l-dopa medications.
Since the discovery more than a decade ago that Parkinson's patients suffer from a profound deficiency of the powerful brain antioxidant glutathione, medical researchers have been actively exploring techniques to administer this naturally-occurring chemical. It is currently used intravenously.
Parkinson's disease is almost certainly caused by oxidative stress aggravated by metal toxicity. People who live in areas where the aluminum content of the drinking water is high have an excessive risk of developing Parkinson's disease. Recent research has linked high aluminum levels in drinking water to acid rain that leaches the aluminum out of the soil and transfers it to the ground water. Other metals are also implicated.
People with a high intake of sugar (mono- and disaccharides) increase their risk of developing Parkinson's disease by a factor of three as compared to people with a more moderate intake.
Diets high in vitamin C and beta-carotene provide significant protection against Parkinson's disease. American researchers have concluded that a high intake of animal fats is associated with a five-fold increase risk.
American researchers have concluded that a high intake of animal fats is associated with a five-fold increase in the risk of developing Parkinson's disease.
Occupational exposure to pesticides and herbicides has also been linked to a significantly higher risk of developing Parkinson's disease.