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Study shows diet supplement may slow early development of symptoms

(11/19/02) Thanks to a small but carefully controlled study, researchers are expressing hope for the use of an over-the-counter diet supplement to slow the early development of symptoms of Parkinson’s disease (PD).

The substance is called Coenzyme Q10. It is easily available at drugstores across the United States.

Despite the favorable results of the small study, doctors warn that patients already taking medications for PD should not take Coenzyme Q10 without checking carefully with their own physicians. The interaction between the diet supplement and pharmaceuticals commonly prescribed for PD is unpredictable.

The 16-month study was conducted under the general direction of Clifford W. Shults, M.D., of the University of California at San Diego. The 80 participants were enrolled at 10 medical centers throughout the United States, including Weill Cornell Medical College in New York City, recipient of a center grant from the Parkinson’s Disease Foundation (PDF). The scientific advisory committee of the project was headed by Christopher Goetz, M.D., head of the movement disorder center at Rush Presbyterian/St. Luke’s Medical Center in Chicago, another recipient of a PDF center grant. The project was sponsored by the National Institute of Neurological Diseases and Stoke (NINDS).

The study design was very simple. The participants were picked from individuals diagnosed with PD, but with symptoms too mild to require levodopa or other prescription pharmaceuticals. After screening, they were divided into four groups on a “double blind” basis (with neither the participant nor the doctor aware of which patient was in which group). One group was assigned to take a small dose – 300 milligrams per day (mg/d) – of Coenzyme Q10. The second and third groups were assigned to take somewhat larger doses – 600 mg/d and 1200 mg/d. The fourth group received a placebo – a pill resembling Coenzyme Q10 but containing none of the substance.

At the end of 16 months of treatment, patients taking 1,200 mg daily of Coenzyme Q10 were significantly better than patients taking placebo, as based on a standard rating scale for measuring PD. Patients in the 300 mg/d and 600 mg/d groups were also better than those in the placebo group, but the difference was not statistically significant. The authors interpreted this result as showing that Coenzyme Q10, taken at 1,200 mg/d, can slow the progression of early PD.

Why Coenzyme Q10 helped the PD patients in this study is not clear. The drug plays a role in cell energy production, and perhaps can boost brain cell function in PD. This idea is, however, speculative, and needs further study. It is possible that Coenzyme Q10 interacts with PD medications, or has some other direct effect on PD symptoms unrelated to slowing disease progression. In this study, it was noted Coenzyme Q10 did not prevent or delay the need for antiparkinson medication any better than placebo. Also, when using a timed tapping device to assess hand function, patients taking Coenzyme Q10 performed no differently than those taking placebo.

Coenzyme Q10 is well tolerated and safe. The major drawback to its use is the expense, estimated at $1,500 to $2,500 a year. This vitamin is an over-the-counter drug, and is not covered by medication plans. The result of this study is promising but further research, involving larger numbers of patients, is needed before Coenzyme Q10 can be recommended as a standard agent for PD.

In the words of Dr. Schults, “This study hasn’t yet proven unequivocally that it will slow the progression of PD. Coenzyme Q10 is not inexpensive, and I don’t recommend that people spend $1,500 to $2,500 a year on a compound that may eventually turn out to be not effective.”

End Parkinson's Disease Foundation information.
  • Coenzyme Q-10 measurably increases the efficiency of cellular energy production, as demonstrated in studies performed at the Massachusetts General Hospital.(1) In addition, it serves as a potent brain antioxidant. These effects explain why major institutions worldwide are vigorously evaluating coenzyme Q10 as a therapeutic aid in brain disorders.
  • Alpha Lipoic Acid provides powerful antioxidant action and regenerates other important brain antioxidants including vitamins E, C, and glutathione. Unlike other antioxidants, alpha lipoic acid is both fat- and water-soluble, greatly enhancing its ability to be absorbed from the gut and penetrate into the brain.(2)
  • N-Acetyl-L-Cysteine (NAC) increases the body’s production of glutathione, one of the brain’s most important antioxidants. NAC itself is a potent antioxidant shown to reduce formation of nitric oxide, a free radical implicated as a causative role in Parkinson’s disease, Alzheimer’s disease, and other neurodegenerative disorders.(3)
  • Bioactive Whey Protein (Immunocal) dramatically increases the body’s production of glutathione. Low levels of glutathione are associated with increased nitric oxide and have been implicated as a causative role in Parkinson’s disease, Alzheimer’s disease, and other neurodegenerative disorders.(4,5)
  • Acetyl-L-Carnitine, like coenzyme Q-10, enhances neuronal energy pro-duction by transporting fuel sources into the mitochondria – the energy producing machinery of the neuron. This particularly benefits damaged brain neurons, which are characterized by decreased energy producing ability. In addition, acetyl-L-carnitine acts as an effective antioxidant and been demon-strated to protect laboratory animals from developing parkinsonism when they are exposed to chemicals known to induce the condition.(4) A report in a recent issue of Neurology found that acetyl-L-carnitine profoundly reduces the rate of progression of Alzheimer’s disease in younger patients.(5)
  • Vitamin E exhibits profound ability to limit free radical damage in the brain – the likely explanation of why it outperformed a highly touted “Alzheimer’s drug” in clinical trials reported in the New England Journal of Medicine.(6) Diets rich in Vitamin E have been shown to reduce the risk of Parkinson’s disease by an incredible 61%,(7) and to dramatically slow disease progression in already-diagnosed patients when supplemented with Vitamin C.(8)
  • Gingko biloba, one of the most extensively studied nutritional supplements for neurodegenerative conditions, directly improves brain metabolism, increases brain blood flow, and provides antioxidant action. In a placebo-controlled, double-blind randomized trial published in the Journal of the American Medical Association, Gingko biloba not only stabilized Alzheimer’s disease; many subjects demonstrated an actual improvement noted in various standardized psychological tests.(9)
  • Vitamin D may have even greater ability to quench brain free radicals than Vitamin E, several studies indicate. Deficiencies of Vitamin D have been found in cases of Parkinson’s, Alzheimer’s, and MS.(10)
  • Vitamin B12 (Methylcobalamin) is critical for maintaining myelin, the protective coat surrounding each neuron. As with Vitamin D, Vitamin B12 deficiency is associated with neurodegenerative conditions.
  • Phosphatidylserine produces marked memory and learning improvements in demented patients, according to research conducted at Stanford University.(11) Like acetyl-L-carnitine and coenzyme Q-10, phosphatidylserine plays an important role in neuronal energy production and chemical communication.
  • Vinpocetine: Clinical trials demonstrate that vinpocetine meaningfully improves the outcome of stroke patients, even when administered long after the initial stroke event. In a 1985 Japanese study, researchers demonstrated improvement in two-thirds of stroke patients receiving vinpocetine.(14) Vinpocetine’s effectiveness in stroke recovery is likely due in part to its remarkable ability to dilate brain arteries, enhancing brain blood flow in patients with cerebrovascular disease. This improves delivery of lifegiving oxygen to marginally functioning areas of the brain. As a potent antioxidant and neuroprotector, vinpocetine limits ongoing brain damage from free radical production.(15) In addition, it increases the flexibility of red blood cells and reduces the tendency of red blood cells and platelets to stick together, further enhancing blood flow to damaged areas of the brain while reducing the risk of subsequent stroke.(15,16) Italian researchers have confirmed the effectiveness of vinpocetine in treating vascular dementia. In a 1987 study published in the Journal of the American Geriatric Society, their report stated, “56 percent of the patients in the vinpocetine group made good to excellent improvement since entering the study.”(17)

    More information on Parkinson's Disease
  1. Schults, C.W., Beal, M.F., Fontaine, K., et al. Absorption, tolerability and effects on mitochondrial activity of oral coenzyme Q10 in parkinsonsian patients, Neurology 50: 793-795, 1998.
  2. Marangon, K., Deveraj, S., Tirosh, O., et al., Comparison of the effect of a-lipoic acid and a-tocopherol supplementation on measures of oxidative stress. Free Radical Biology and Medicine 27(9/10): 1114-1121, 1999.
  3. Pahan, K., Sheikh, G.S., Nmboodri, A.M.S., et al., N-acetyl cysteine inhibits induction of NO production by endotoxin or cytokine stimulated rat peri-toneal macrophages, C6 glial cells and astrocytes. Free Radical Biology and Medicine 24(1):39-48, 1998.
  4. Canals S, Casarejos MJ, De Bernardo S, Rodriguez-Martin E, Mena MA. Nitric Oxide Triggers the Toxicity due to Glutathione Depletion in Midbrain Cultures through 12-Lipoxygenase. J Biol Chem. 2003 Jun 13;278(24):21542-9.
  5. Mytilineou C, Kramer BC, Yabut JA. Glutathione depletion and oxidative stress. Parkinsonism Relat Disord. 2002 Sep;8(6):385-7.
  6. Steffen V. Santiago, M., de la Cruz, C.P., et al., Effect of intraventricular injection of 1-methyl-4-phenylpridinium protection by acetyl-L-carnitine. Human Exp Toxicol 14:865-871, 1995.
  7. Thal L.J., Carta A. Clarke, W.R., et al., A 1-year multicenter placebo-con-trolled study of acetyl-L-carnitine in patients with Alzheimerâs disease. Neurology 47:705-711, 1996.
  8. Sano, M., Ernesto, C., Thomas, R.G., et al., A controlled trial of selegeline, alpha-tocopherol, or both as treatment for Alzheimerâs disease. N England J Med 336:1216-22, 1997.
  9. Golbe, L.I., Farrell, T.M., David, P.H., Case-control study of early life dietary factors in Parkinsonâs disease. Arch Neurol 45(12): 1350-3, 1988.
  10. Fahn, S., The endogenous toxin theory of the etiology of Parkinsonâs dis-ease and a pilot trial of high-dose antioxidants in an attempt to slow the progression of the illness. Ann N Y Acad Sci 570:186-96, 1989.
  11. Le Bars, P., Katz, M.M., Berman, N., et al,. a Placebo-Controlled, Double-blind Randomized Trial of an Extract of Gingko Biloba for Dementia. JAMA 278(16): 1327-32, 1997.
  12. Sardar, S., Chakraborty, A., and Chatterjee, M., Comparative effectiveness of vitamin D3 and dietary vitamin E on peroxidation of lipids and enzymes of the hepatic antioxidant system in Sprague-Dawley rats. Int J Vitam Nutr Res, 66(1):39-45, 1996.
  13. Crook, T.H., Tinklenberg, J., Yesavage, J., Effects of phosphatidylserine in age-associated memory impairment. Neurology 41:644-49, 1991.
  14. Otomo, E., Ataractic, J., Arakai, G., et al., comparison of Vinpocetine with ifenprodil tartrate and dihydroergotoxine mesylate treatment and results of long-term treatment with Vinpocetine. Curr Therapeut Res, 37:811-821, 1985.
  15. Tamaki, N., Kusunoki, T., Matsumoto, S., The effect of Vinpocetine on cerebral blood flow in patients with cerebrovascular disease. Ther Hung, 33:13-21, 1985.
  16. Olah, V.A. Balla, G., Balla, H., et al., An in vitro study of the hydroxl scavenger effect of caiton. Acta Paediatr Hung, 30: 309-316, 1990.
  17. Osawa, M., Maruyama, S., Effects of TCV-3B (Vinpocetine) on blood viscosity in ischemic cerebrovascular disease. Ther Hung, 33: 7-12, 1985.
  18. Hayakawa, M., Comparative efficacy of Vinpocetine, pentoxyifylline and nicergoline on red blood cell deformability. Arzneinmittelforschung, 42: 108-110, 1992.