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.
Incidence and Symptoms
With no known cause, Parkinson’s disease affects about 1% of the population over the age of 60 years in the United States. It is more common among men than women and also seems to be more widespread in northern countries. The incidence of the disease increases with age although aging itself is not believed to be a causative factor. Parkinson’s disease is rarely inherited and less than 1% of all cases are thought to have a genetic component. At this time there is no medical cure for the condition, but drugs that alleviate the symptoms and slow the progress of the disease are available. L-dopa, the mainstay of current drug therapy, was introduced in 1970 and since then hundreds of research papers have been published on the disease.
The main symptom of Parkinson’s disease is a pronounced tremor affecting the extremities – notably the hands, chin or lips. The tremor is most evident at rest and disappears with movement and sleep. Other characteristic symptoms of Parkinson’s disease are stiffness or slowness of movement, a shuffling walk, stooped posture, and difficulties in performing simple tasks. Memory impairment and cognitive dysfunction are rarely encountered in early stage Parkinson’s disease. Depression is, however, a common feature and about 30% of Parkinson’s disease victims eventually develop Alzheimer’s disease or other forms of dementia.
Environmental and Dietary Factors
Parkinson-like symptoms can also 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 In some cases, drug-induced Parkinson’s disease may be halted or reversed if the drug is promptly withdrawn.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.
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. Other metals, notably manganese, cadmium, copper, and mercury (from dental amalgams) have also been implicated as causative factors in the development of Parkinson’s disease.
Alternative Treatment
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.
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.