A very dramatic story about the effects of L-Dopa on twenty patients with severe Parkinson’s disease is contained in Oliver W. Sack’s book Awakenings. Between 1916 and 1927, nearly five million people fell victim to encephalitis lethargica (sleeping sickness). A third of those affected died either in a coma or in a profound state of sleeplessness which could not be alleviated even with sedatives. Patients who survived were often in a condition of being conscious and aware but not fully awake. They were unmotivated and seemed like zombies. They commonly developed such symptoms of Parkinson’s disease as tremor, rigidity, compulsive movements, and profound states of nonmovement.
When, in 1967, it was realized that L-Dopa is an effective treatment for Parkinson’s disease, Dr. Sacks treated twenty of these sleeping sickness
victims (who were then quite old and had been zombies for nearly their entire lifetime). The book is a moving description of their awakenings with L-Dopa and subsequent developments, some of which were tragic. The poor results with L- Dopa, as experienced by some of these patients, is probably
due to the autoxidation of L-Dopa, resulting in the production of 6-hydroxy-dopamine. The latter autoxidizes, producing free radicals and hydrogen peroxide, which damage dopaminergic nerve cell receptors. This problem could probably have been avoided, or at least mitigated, by giving the patients large doses of antioxidants (such as vitamins E, C, B-1, B-5,
zinc, selenium and Hydergine®) along with the L-Dopa.
Warning: People who are taking L-Dopa for Parkinson’s disease should not take vitamin B-6 supplements unless advised to do so by their physician. Vitamin: B-6 helps converts the amino acid L-Dopa to the neurotransmitter dopamine in the brain where such conversion is desired, but it also helps
to convert L-Dopa to dopamine peripherally (outside of the brain) in the remainder of the body. If a Parkinson’s patient takes large doses of B-6, so much L-Dopa may be converted peripherally that there may be undesired peripheral side effects while, at the same time, not enough L-Dopa may be
available to adequately elevate dopamine levels in the brain. (L-Dopa crosses the blood-brain barrier, the selective membrane surrounding the brain and spinal cord, but dopamine does not.) This can result in a temporary worsening of Parkinsonism symptoms.
Most of the persons we know who are currently participating in life extension experiments do not have Parkinson’s disease, and many of these non-Parkinsonism patients have had a good response to 1/4, to1/2 gram of L-Dopa at bedtime (as indicated by the fat loss and muscle buildup resulting from L-Dopa’s stimulation of growth hormone release by the pituitary gland), even though they were also taking large doses of vitamin B-6 at the same time as they were taking L-Dopa.
Schizophrenia is thought by many researchers to involve errors in dopamine metabolism. The phenothiazines (most of which are antioxidants), used widely as treatment for schizophrenia, prevent excessive sensitivity in response to dopamine by blocking the dopamine receptors. Sometimes in long-term use of phenothiazines, uncontrollable movements in the jaw, tongue, and face (a disorder known as tardive dyskinesia) develop due to inadequate cholinergic stimulation. Recently, choline has been used successfully to treat tardive dyskinesia. Other cholinergics (such as Deaner® or lecithin) might also be effective therapy for this disorder.
In a recent study, old rats (the age equivalent of a human 80 years old) given L-Dopa regained the swimming abilities of healthy young rats. Swiss male mice fed L-Dopa in the life- span study of Dr. George C. Cotzias had significant life extensions. (Dr. Cotzias developed L-Dopa therapy for Parkinson’s disease.) However, in these mice there was a high initial mortality among the mice given the highest dose of L-Dopa (they were not given gradually increasing doses).
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