Halt the stealth threat of Parkinson's disease: advanced protection for the aging brain.
Vitamin B6 in physiologically active form is the prerequisite for the production of dopamine. Deficiencies and disorders in B vitamin and folate metabolism have thus been implicated in many neurological disorders, including PD, and studies as early as the 1970's were directed at demonstrating the effects of supplementation--initially with discouraging results. (52-54)
As our understanding of the role of the toxic amino acid homocysteine grew, however, more targeted and mechanism-based studies became possible. Homocysteine levels are closely related to folate, vitamin B6, and vitamin B12 status, and elevated homocysteine is found in cardiovascular disease and a variety of neurological and psychiatric disturbances, including PD. (55-57) Paradoxically, levodopa treatment of PD can itself lead to elevations in homocysteine, potentially worsening the condition. This has prompted researchers to recommend B complex supplements in those taking the drug. (58)
Definitive demonstration of the value of this approach came from Singapore in 2005, where neurologists supplemented PD patients who were stable and on their best doses of levodopa with pyridoxine, a common form of vitamin B6. Mean motor and activities of daily living scores improved significantly following supplementation, and deteriorated again when the supplements were stopped. (59) Low serum folate is also found in PD patients, especially those taking levodopa; (57) Canadian researchers have demonstrated that a folate/B12 supplement could decrease plasma homocysteine levels in patients taking levodopa. (60)
A review paper in 2007 points to recent work with the active form of vitamin B6, pyridoxal-5' phosphate (P5P), noting that a number of neurological disorders including PD offer attractive therapeutic targets for this substance. (61) Because of the association of elevated homocysteine and its deleterious effects with both PD itself and levodopa therapy, supplementation with folate, B6, and B12 is warranted. (62-65)
One note of caution regarding B6 supplements is if a PD patient is being treated with levodopa alone without the decarboxylase inhibitor carbidopa. Vitamin B6 may cause levadopa to convert to dopamine in the bloodstream before it crosses the blood-brain barrier (where it beneficially converts to dopamine in the brain). For safety's sake, it is best to take vitamin B6 supplements at a time of the day furthest from the last dose of a levadopa (L-dopa)-containing medication and to have one's blood tested periodically to make sure that excess dopamine does not accumulate in the bloodstream.
Carnitine serves as a co-factor in fatty acid metabolism--it helps to "shuttle" large fat molecules into the cellular powerhouses known as the mitochondria, where they are metabolized for energy. This makes carnitine a valuable weapon against PD. (5), (66) A small but burgeoning body of data indicates carnitine as a promising preventive for PD through its support of brain energy management.
Researchers at Mount Sinai Medical Center have successfully prevented experimentally-induced PD in monkeys by pre-treating them with acetyl-L-carnitine (ALC), a readily-absorbed form of the nutrient. (67) Italian researchers have led the way in studies of carnitine as a neuroprotective agent in the brains of methamphetamine users, who develop an acute form of brain injury resulting from the same basic mitochondrial destruction and free radical damage observed in PD. (66), (68) This work has been extended in similar studies by researchers at the US National Center for Toxicological Research. (69)
In the most exciting recent development in this area of research, Chinese nutritional scientists in Shanghai explored the combination of ALC with another energy-related nutrient, lipoic acid, in preventing PD-like changes in human neural cells in culture. (70) They found that either nutrient, or the combination, applied for 4 weeks prior to a PD-inducing chemical, protected the cells from mitochondrial dysfunction, oxidative damage, and accumulation of the dangerous alpha-synuclein protein characteristic of PD.
Most notably, the combination of supplements was effective at 100- to 1,000-fold lower concentrations than were required for either acting alone--powerful evidence for a synergy that led the researchers to conclude, "This study provides important evidence that combining mitochondrial antioxidant/nutrients at optimal doses might be an effective and safe prevention strategy for PD." (70)
According to internationally-noted Israeli neuroscientist Sylvia Mandel, "Tea consumption is inversely correlated with the incidence of dementia and Al zheimer's and Parkinson's diseases." (71) Green tea contains valuable antioxidant polyphenols known to be protective against a host of chronic and age-related conditions.
This has given rise to a tremendous scientific interest in green tea and its active compound epigallocatechin gallate or EGCG as a neuroprotectant in PD, especially because these compounds penetrate into brain tissue extremely well compared to many drugs. (72-74) Israeli researchers showed in 2001, for example, that they could prevent the cellular changes associated with PD in mice by pre-treating them with either green tea extracts or EGCG ahead of inducing the condition by chemical injection, (73) work that has subsequently been repeated and extended in laboratories around the world. (75-80) The Israeli team also demonstrated that green tea extracts can prevent activation of the inflammation-producing nuclear factor-kappaB (NF-kB) system in brain cell cultures triggered to develop PD-like changes. (81) EGCG's specific anti-inflammatory properties have been further shown to protect cultured brain tissue from the loss of dopaminergic cells as well. (16) An entirely distinct component of green and black teas, L-theanine, is a unique amino acid that can cross the blood-brain barrier. (82) Korean scientists have recently shown it may prevent the dopaminergic cell death characteristic of PD. (83)
Another potential benefit of green tea extracts is their ability to sustain dopamine levels in ailing brain tissue, reducing the severity of symptoms. (84)
The multiple beneficial compounds found in green tea form a combination therapy all their own, maximize their neuroprotective effects in PD and other neurodegenerative conditions. (71), (80), (85-89)
Since dopamine itself is an oxidant compound which can contribute to the early demise of its own neurons, scientists have studied the antioxidant potential of resveratrol to prevent this paradoxical destruction. They found that human neural tissue treated with dopamine underwent rapid cell death as a result of loss of mitochondrial function, but that exposing the cells to resveratrol for just one hour prior to dopamine treatment prevented cell loss and preserved mitochondrial function. (90) Canadian scientists showed in 2008 that they could prevent neuronal cell death caused by inflammation through the use of resveratrol. (91)
That anti-inflammatory action was further dramatically explored by Chinese researchers, who first administered a PD-inducing chemical to rats, and then gave them resveratrol orally each day for 10 weeks. (92) They found that even as early as 2 weeks into supplementation, the diseased rats demonstrated significant improvement in their movement disorders, and examination of their brains showed marked reduction in mitochondrial and dopaminergic cell damage. Remarkably, they also found a reduction in expression of the inflammatory markers cyclooxygenase-2 (COX-2) and tumor necrosis factor-alpha (TNF-alpha). They were led to conclude that "resveratrol exerts a neuroprotective effect on [a chemically]-induced Parkinson's disease rat model, and this protection is related to the reduced inflammatory reaction."
As with green tea extracts, it appears that resveratrol's promise for PD prevention may reside in its multi-modal mechanisms of action, targeting oxidative stress, inflammation, and other cellular processes fundamental in regulating brain function. (93)
The explosion of knowledge about the many interrelated probable causes of Parkinson's disease in the past decade has led to a number of other nutrient molecules' being explored for their neuroprotective, anti-parkinsonian potential. Vitamin D, for example, a known neurohormone with neuroprotective effects throughout the life span, has been shown to prevent many of the changes associated with PD in laboratory and animal studies; it is also known to be deficient in a large proportion of PD sufferers. (94-99) Curcumin, a derivative of the spices turmeric and cumin, is a natural inhibitor of inflammation through its potent modulation of the inflammatory NF-kappaB system; it prevents chemically-induced changes in lab models of PD, and exerts significant neuroprotection. (100-107) And the pineal hormone melatonin, an antioxidant in its own right, may help to preserve cells' ability to make dopamine and to reduce accumulation of destructive alpha-synuclein proteins. It is also invaluable as a sleep aid for PD victims, who often suffer from distressing sleep disturbances. (108-114)
While its precise cause remains unknown--and there is no cure--aging is the single most important risk factor for Parkinson's disease (PD). Symptoms manifest in PD victims as early as age 50 (earlier in rare instances). The risk of onset continues to rise with advancing age. Incidence increases dramatically at age 60. Slowed movement, tremors, mild cognitive impairment, and difficulty standing up are the early warning signs. End-stage PD is marked by dementia, near-total immobility, personality and mood disorders, and death. These are the result of multiple, interacting destructive processes triggered by oxidant stress, mitochondrial dysfunction, and inflammation. Together these processes selectively and irreversibly destroy vital movement-controlling cells deep in the brain, resulting in loss of control and gradual decline in movement and activity. Nutritional interventions acting through multiple mechanisms can slow or prevent the accumulation of brain cell damage that produces Parkinson's disease. In particular, nutrients that enhance brain energy utilization, prevent mitochondrial dysfunction, protect against oxidant damage, and tame inflammation are among the leading contenders for anti-Parkinson's therapies. The most promising among these include creatine, omega-3 fatty acids, coenzyme Q10, B vitamins (particularly B6 and pyridoxal-5'phosphate), carnitine, lipoic acid, green tea extract, and resveratrol.
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By Julius Goepp, MD
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