L-Dopa (Levodopa) exists physiologically as a naturally occurring amino acid (L-3, 4-dihydroxyphenylalanine). Once thought as being inert, or biologically inactive, studies in the later 1920’s and early 30’s proved that both the D- and L-forms of Levodopa were significant in effects witnessed on both blood glucose levels, and arterial blood pressure stabilization.  Future studies would also suggest L-Dopa’s possible prominence in enzymatic conversion to Dopamine levels in the brain and its ability to enhance cognitive functioning; especially concerning its positive effects on individuals suffering from Parkinson's Disease and Schizophrenia.
Being a neurotransmitter, Dopamine is critical in numerous central nervous system activities. The reward recognition, as well as cognitive and physical distress mechanisms in human biology have been directly associated to this inhibitory neurotransmitter. The abovementioned parkinsonian patients are characterized by the extreme depletion of dopamine levels within the brain. These persons are often marked with symptoms ranging from minor trembling to rigidity, prolonged movement of the limbs, and even depression. Studies dating back to the early 1970’s have highlighted dopamine activity and its effect on brain dysfunction and activities relating to specific diseases; primarily Parkinson’s.
It has been generally accepted by the medical community that L-Dopa’s primary use may lye within the realms of brain neurotransmitter replacement therapies.
Tyrosine and phenylalanine are direct precursors to dopamine levels within the brain, thus suggesting persons achieve adequate intakes of both of these particular amino acids. (See Tyrosine and Phenylalanine) There are, however, no specific foods which contain direct sources or provide direct dopamine release within the body. A food graph has been omitted for this nutrient.
It is suggested that the supplemental intake of Vitamin B6 (5 - 10 grams daily) be administered during prolonged supplementation of L-Dopa and dopamine-containing drugs.  This amount of Vitamin B6 is often recommended for the prevention of levodopa-induced pyridoxine deficiency.
High protein diets are often ill-advised during L-Dopa supplementation, as foods high in protein compete for the absorption of levodopa.
Parkinson’s disease has garnered much public attention within the last decade. This condition is a growing epidemic and effects diverse individuals located in each stratum of our ever-growing, worldwide societies. In America, some 60,000 cases of this brain disease will be diagnosed this year. Currently, there are no cures or known drugs which halt the progression of this particular neurodegenerative disease; however, therapies do exist to lessen the most severe of Parkinson’s Disease symptoms. 
Dopamine depletion within certain areas of the brain is believed to cause the majority of signs and symptoms associated with the development of Parkinson’s disease. The neuron responsible for the brain’s release of dopamine is the substantia nigra. This dopamine releasing nuclei sends dopamine axons to the basal ganglia area of the brain, where dopamine is needed for smooth, voluntary movement. When an estimated 80 percent of these specific neurons (substantia nigra) are damaged, the beginnings of Parkinson’s disease is eminent. This is when therapeutic protocols are employed to lessen the severity of onset.
L-Dopa (levodopa) has become a “gold” standard in therapy when used in conjunction with traditional synthetic medicines for Parkinson’s sufferers. This nutrient allows for ingested forms of oral dopamine to cross the brain’s blood-brain-barrier. These assisted increases of dopamine concentration in the brain by supplemental dopamine account for improved neurological conduction and muscle functioning. The New England Journal of Medicine has also recommended L-Dopa use in Parkinsonian patients when there is a consistent profile of adverse events arising from this degenerative condition. 
Various supplemental forms of L-Dopa may also treat another classified neurological disease as well. A Dopamine hypothesis of schizophrenia (also referred to as the biochemical theory of schizophrenia) exist, stating that the over-activity of dopamine production within the brain causes schizophrenia.  This theory is predicated upon the scientific knowledge that antipsychotic drugs lessen the activity of dopamine by blocking certain receptors, and by examining the drugs that boost dopamine functioning in the brain, such as amphetamines; all of which seem to worsen the illness and activity in schizophrenic patients. Comparative analysis with alive and after death (post-mortem) brains have also substantiated the claim that schizophrenic individuals possess far more dopamine receptors than healthy people.
Other possible uses for levodopa therapy include the treatment of herpes zoster (shingles) and restless leg syndrome. Drug addiction has also been linked to the mesolimbic dopamine system. This dopamine pathway serves as the abovementioned pleasure/reinforcement, or reward systems, of the human body. Drugs classified as stimulants and/or depressants seem to directly or indirectly activate areas of this subsystem. More research is, however, needed to validate these preliminary findings.
There is no Recommended Dietary Allowance for L-Dopa. Dosages generally vary and are dependant upon the type of medicine used; as well as individual tolerance. It is recommended that the different forms of supplemental L-Dopa be taken on an empty stomach for optimal absorption. The table below is standard for levodopa treatment for Parkinson’s Disease.
Oral dosages for Levodopa Tablets:
|Dosges:||Adults and Teenagers||Children up to age 12|
|250 milligrams 2-4 times per day, w/o exceeding 8 grams per day||(Rare) Use and dosage must be determined by physician|
- It is advised that dosages for supplemental L-, or D-Dopa be personally restricted and not exceeded. Again, dosages will vary by individual and are solely dependent upon the dysfunction / disease which is being treated, as well as physician recommendations for supplementation protocol -
Deficiencies of this particular nutrient are coupled with the usage section of this monograph.
Recent in vitro studies suggest that supplemental L-Dopa may damage certain neurons (dopaminergic) similar to those found in the human brain tissue; especially in persons suffering from Parkinson’s disease.  This study is often refuted by varying clinical applications, all of which seemingly agree that L-Dopa does not hasten the progression of Parkinson’s disease, but rather improves the overall physiological functioning in Parkinson’s patients.
Levodopa toxicity has only been known to occur in patients who considerably exceed a physicians recommended dosages. In a 1997 study in Sweden, two Parkinson disease patients exceeded their recommended daily dosages by nearly 500 - 1000 mg/day, from a pre-established dosage of 1500 - 2000 mg/per day. This was the minimum dosage administered by physicians to ward off the symptoms associated with Parkinson’s disease in these individuals.
Both persons did not consent to doctors orders, which were to immediately reduce their elevated dosages. Subsequently, these individuals were found to be physiologically dependant upon the adverse effects of this “mega” dosing, such as; abnormally increased and sometimes uncontrollable activity or muscular movements (hyperkinesis), anorexia, and fixed euphoria with hallucinogenic states. 
1. Hornykiewicz O. L-Dopa: “From a biologically inactive amino acid to a successful therapeutic agent.” A Historical Review Article. Institute for Brain Research, University of Vienna, Vienna, Austria. Amino Acids 2002; 23(1-3):65-70.
2. Trovato A, et al. Drug-nutrient interactions. Am Family Phys 1991;44:1651-8.
3. The National Parkinson Foundation homepage. “About Parkinson’s Disease.” Apr. 12, 2005. Copyright 1996-2004, National Parkinson Foundation, Inc.
4. Fahn, S. The New England Journal of Medicine, Dec. 9, 2004; vol 351: pp2498-2508.
5. Kornhuber HH, Kornhuber J, Kim JS, Kornhuber ME. “A biochemical theory of schizophrenia.” [Article in German] Nervenarzt, 1984 Nov;55(11): 602-6.
6. Lewitt PA, Nyholm D. “New Developments in levodopa therapy.” Dept of Neurology, Psychiatry and Behavioral Neuroscience, Wayne State University School of Medicine; Detroit, MI, USA. Neurology, 2004 Jan 13;62(1 Suppl 1):S9-16.
7. Spigset O; von Scheele C. Division of Clinical Pharmacology, Norland University Hospital UmeAa, Sweden. [Abstract Article] Pharmacotherapy, 1997 Sep, 17:5, 1027-30.