Botanical and Supplements
Amino Acid Therapy
As we discussed in the section on Amino Acid Therapy, the only way to address the underlying neurotransmitter imbalances associated with Parkinson’s disease-like RND symptoms is to take the proper balance of L-dopa in conjunction with 5-HTP, L-tyrosine, L-cysteine and necessary cofactors to restore optimal neurotransmitter function. Every single person requires a unique combination of nutrients to fully address their unique underlying imbalances and eliminate their PD-like RND symptoms.
This can only be accomplished by working with a provider trained in the proper use of amino acid therapy and is imperative for long term success. Please contact us to get started.
B-Vitamins and Parkinson’s
Certain B-vitamins are known to play a role in the initiation and progression of Parkinson’s disease. There is a close link between the toxic amino acid homocysteine and cardiovascular disease as well as a variety of neurological and psychiatric disorders, including Parkinson’s disease. In addition, the medical use of L-DOPA can also lead to depletion of folate and vitamin B6 and elevated homocysteine. Homocysteine levels are closely linked to folate, vitamin B6 and vitamin B12, so supplementation with these B-vitamins is warranted to lower homocysteine levels and keep them within normal limits.
In particular, several studies have shown that vitamin B6 (pyridoxine or pyridoxal-5-phosphate) may be particularly important for those with Parkinson’s disease. One study showed that people with Parkinson’s disease who were stable on their best doses of L-DOPA showed a significant improvement in mean motor skills and activities of daily living following supplementation with vitamin B6. These benefits disappeared when the vitamin B6 supplements were stopped. Another study revealed that inadequate vitamin B6 intake may increase the risk of developing Parkinson’s disease by 50%.
Once more, those people that have taken carbidopa at any time in their past are very likely to have an extreme deficiency of vitamin B6 due to the action of carbidopa. Carbidopa irreversibly binds to pyridoxal-5-phosphate (P5P) and P5P dependent enzymes; this causes permanent deactivation of these enzymes. Aromatic L-amino acid decarboxylase (AADC) is one of those P5P dependent enzymes (recall this enzyme catalyzes the synthesis of both serotonin and dopamine in the periphery (i.e., outside the central nervous system). This is a unique situation where carbidopa permanently takes out the enzymes and the substrate (vitamin B6) required for activating the enzymes. This produces a profound long-term deficiency of vitamin B6. This vitamin B6 deficiency cannot be corrected until the carbidopa is discontinued.
As discussed earlier, Parkinson’s disease is a neurodegenerative disorder that can result from mitochondrial dysfunction and oxidative stress. Coenzyme Q10 (CoQ10) also known as ubiquinone or ubiquinol, is both a potent antioxidant and it can help reverse mitochondrial dysfunction, which offers protection to neurons. Numerous studies in both animal and human models of Parkinson’s disease have demonstrated that coenzyme Q10 can protect dopaminergic neurons. Once more, research has shown that CoQ10 is deficient in people with Parkinson’s disease, suggesting a systemic deficiency state.
Coenzyme Q10 acts as a critical energy carrier in mitochondrial electron transport. It also functions as an antioxidant to inhibit lipid peroxidation that kills dopamine producing neurons. According to a study in a 2002 issue of Neurochemistry Research, scientists believe that coenzyme Q10 works by improving cellular energy production, preventing oxidative stress and inhibiting neuronal cell death.
Groundbreaking research on using CoQ10 with Parkinson’s disease was first introduced at the 2002 annual meeting of the American Neurological Association (New York City, Oct. 13-16) and simultaneously published in the journal Archives of Neurology. For the first time, these researches showed that oral coenzyme Q10 can actually slow the progression of Parkinson’s disease.
This multi-center clinical trial randomly assigned 80 people with early stage Parkinson’s disease, who were not yet being treated, to receive either placebo or CoQ10 at daily doses of 300, 600 or 1200 mg for 16 months or until disability required drug treatment. All of the coenzyme Q10 doses were safe and well-tolerated during the 16-month trial.
The patients in the study were scored using the standard Unified Parkinson Disease Rating Scale (UPDRS), to establish baseline scores for their basic motor skills, mental status, mood and behavior, and ability to perform daily living activities. Since the scale is designed to measure disease progression, lower UPDRS scores indicate better performance. The results were compelling with a mean change of 11.99 for the placebo group, 8.81 for the 300 mg/day group, 10.82 for the 600 mg/day group and 6.69 for the 1200 mg/day group.
Basically, these findings demonstrate that coenzyme Q10 supplementation at 1200 mg/day resulted in 44% less mental and physical disability than placebo. In addition, the authors reported “the greatest benefit was seen in activities of daily living: dressing, bathing, eating and walking.” The patients in the 1200 mg/day group were better able to function, and maintained greater independence for a longer time than those in the placebo or other Co10 dosing groups.
The authors concluded: “The causes of Parkinson’s disease are unknown, [but] evidence suggests that mitochondrial dysfunction and oxygen free radicals may be involved in its pathogenesis. The dual function of coenzyme Q10 as a constituent of the mitochondrial electron transport chain and a potent antioxidant suggest that it has the potential to slow the progression of Parkinson’s disease.” Two years later the same researchers showed that dosages up to 3000 mg/day of ubiquinone were safe and well tolerated, though plasma levels reached a plateau at 2400 mg/day.
Another more recently published study showed that the combination of CoQ10 and creatine produced additive neuroprotective effects against dopamine depletion in the area of the brain affected by Parkinson’s disease. There was also a reduction in the loss of tyrosine hydroxylase producing neurons in the substantia nigra (recall tyrosine hydroxylase is a key enzyme involved in the production of dopamine and is used as a marker for dopaminergic neurons). Once more, CoQ10 plus creatine resulted in reduce lipid peroxidation, which represents decreased damage to cell membranes. The study authors concluded, “These findings suggest that combination therapy using CoQ10 and creatine may be useful in the treatment of neurodegenerative diseases such as Parkinson’s disease.”
As for dosing, a person with Parkinson’s disease may consider starting at 300 mg/day and then increase to 600 mg/day two weeks later. If any prescription drugs are being taken, it is important to make sure this high dose of coenzyme Q10 will not create the need for a dosing adjustment. For instance, if Coumadin is being used, the weekly or bi-weekly coagulation blood tests that Coumadin patients are supposed to have can determine if additional Coumadin is needed.
After taking 600 mg/day of CoQ10 for two weeks, a person with Parkinson’s may want to increase the dose to 900 mg/day, and again make sure there is no prescription drug interference. After the 900 mg/day dose has been established as safe, the person with Parkinson’s can increase the dose of CoQ10 to 1200 mg/day. For maximum absorption, always take CoQ10 with the fattiest meal of the day.
It is important to keep in mind that the research to date shows that coenzyme Q10 does not reverse Parkinson’s disease, nor does it alleviate symptoms. However, the research does show that CoQ10 administration is neuroprotective and slows the disease progression. Therefore, CoQ10 supplementation may provide a great adjunctive therapy to be used along with amino acid therapy and/or as a preventative measure.
Studies have shown that the part of the brain affected most by Parkinson’s disease – the substantia nigra – contains high levels of the vitamin D receptor. This indicates the normal function of the substantia nigra may be dependent upon adequate vitamin D levels.
Several studies have found a correlation between insufficient levels of vitamin D and the development of Parkinson’s disease. The authors of one such study noted that, “We found that vitamin D insufficiency may have a unique association with Parkinson’s, which is intriguing and warrants further investigation.” In laboratory as well as animal studies, vitamin D has been shown to be neuroprotective and prevent many of the changes associated with Parkinson’s disease.
While that research is ongoing, anyone concerned about the risk of Parkinson’s disease or those that are already exhibiting symptoms should have their vitamin D levels checked (the test is called 25-hydroxy vitamin D) and supplement accordingly. The ideal range for 25-hydroxy vitamin D is 50-60 ng/ml. Research shows that most adults need between 4000-8000 IU/day of vitamin D3 to obtain this blood concentration.
Creatine is an amino-acid like compound that helps shuttle energy into muscle tissues and is also critical to overall cellular energy metabolism. Research has shown that creatine deficiency in the brain is associated with neurological damage, which has led researchers to explore its potential as a neuroprotective agent. In fact, several animal models have shown creatine to be effective in preventing or slowing the progression of Parkinson’s disease.
The first clinical study of creating in humans was published in 2006. This study looked at 200 subjects who had been diagnosed with Parkinson’s disease within 5 years, but who did not require medication for symptom management. The study participants were randomly assigned to receive either 10 grams of creatine per day, the drug minocycline (200 mg/day) or placebo for 12 months. They were monitored using the Unified Parkinson’s Disease Rating Scale (UPDRS).
Both creatine and minocycline performed well, but the creatine group showed significantly better tolerability (91%) versus the minocycline group (77%). This work was followed up by a 2008 study that showed no safety or tolerability issues with creatine at this dosage over 18 months.
What makes these studies so interesting is that they involved people that already been diagnosed with Parkinson’s disease, which means that much of the damage to the dopaminergic neurons had already occurred. It is likely that creatine may offer superior benefits when used as a preventative agent due to its neuroprotective effects.
Once more, researchers from the Department of Neurology and Neuroscience at the Weill Medical College of Cornell University have discovered that coenzyme Q10 and creatine produce additive neuroprotective effects against dopamine depletion and the loss of tyrosine hydroxylase neurons following chronic administration of a neurotoxic agent in a rat model of Parkinson’s disease. These findings indicate that CoQ10 and creatine may be useful for neuroprotection in Parkinson’s disease via their effects on improving mitochondrial function, cellular energy metabolism and antioxidant effects.
Omega-3 Essential Fatty Acids
As we discussed earlier, inflammation contributes to the progression of neurodegeneration in Parkinson’s disease. Therefore, reducing and/or preventing inflammation in the brain could be a way to control damage to dopaminergic neurons. Omega-3 fatty acids have been shown to beneficially modulate the inflammatory process; in addition, their concentration in nerve cell membranes is known to decrease with age and oxidative stress, as well as in neurodegenerative disorders such as Parkinson’s disease.
In animal models, omega-3 essential fatty acids have shown a remarkable ability to prevent neuronal damage, delay the onset of Parkinson’s disease and/or decrease the rate of disease progression. In one particular study, Canadian researchers either gave mice omega-3 supplementation or placebo for 10 months prior to injecting them with a chemical that produces Parkinson’s disease. The placebo group showed a rapid loss of the dopaminergic cells of the substantia nigra and a dramatic decrease in dopamine levels in brain tissue. However, these effects were prevented entirely in the omega-3 supplemented animals.
In another animal study, researchers showed that the omega-3 fatty acid docosahexanoic acid (DHA) could reduce the severity or delay the development of L-DOPA induced dyskinesias in monkeys with Parkinson’s disease. DHA administration reduced these negative effects whether or not it was given before or several months after the initiation of L-DOPA. The researchers concluded that “DHA may represent a new approach to improve the quality of life of Parkinson’s disease patients.”
Based on the growing body of research supporting the use of omega-3 essential fatty acids (especially DHA) in the prevention of Parkinson’s disease, as well as the beneficial role omega-3 fatty acids have in reducing inflammation, it seems prudent to supplement these inflammation-fighting compounds daily.
Green tea and its active compound epigallocatechin gallate (EGCG) have been extensively studied for their neuroprotective qualities in Parkinson’s disease. In fact, it has been found that the compounds in green tea penetrate the brain tissue better than many drugs used for Parkinson’s disease.
Green tea extracts and EGCG have been shown to prevent cellular changes associated with Parkinson’s disease in mice by pre-treating them ahead of inducing Parkinson’s disease by chemical injection. Green tea extracts as well as ECGC have also been found to prevent inflammation in brain cells triggered to develop Parkinson’s disease-like changes in addition to protecting the loss of dopaminergic cells. Once more, L-theanine (a compound found in green and black teas) has been shown to prevent dopaminergic cell death associated with Parkinson’ disease.
Thus, green tea provides a multitude of beneficial compounds that can provide neuroprotective effects in Parkinson’s disease and should be consumed daily.