Written by Greg Arnold, DC, CSCS. Those who supplemented with 500 mg of inosine for 24 months saw a significant (63.9%) reduction in test points that measures the progression of Parkinson’s disease, compared to placebo. 

Parkinson Disease is characterized by tremors, slowness of movement, and difficulty with balance. The condition affects more than 1.5 million Americans, with 60,000 new cases each year (1) and healthcare system costs of more $5.6 billion per year (2). While research has started to find natural approaches to lowering the risk of Parkinson Disease, such as having healthy blood levels of vitamin D (3), another option may be in supplementing with inosine.

Inosine is the precursor to a type of salt called urate, which has shown promise as an antioxidant (4) and helping maintaining nerve health (5). A 2014 study (6) involved 75 patients (34 men, 41 women) with an average age of 62 who were diagnosed with “early Parkinson’s Disease not yet requiring symptomatic treatment” and urate blood levels below 6 milligrams/deciliter. They received one of three treatments for 24 months:

  • 500 milligrams of inosine taken once daily, designed to produce “mild” urate levels in the urine between 6.1-7.0 milligrams/deciliter (24 subjects)
  • 500 mg inosine taken two to three times daily, designed to produce “moderate” urate levels in the urine between 7.1-8.0 mg/dL) (26 subjects)
  • Placebo pills designed to have no effect of urate levels in the urine (25 subjects)

Over the 24-month study period, 17 “serious” adverse events were reported, but there was no significant difference between the two inosine groups and the placebo group. No subjects withdrew because of adverse events, and early stages of kidney stones (“symptomatic urolithiasis”) was the most serious side effect. Regarding Parkinson Disease progression, using a measure of progression called the Unified Parkinson Disease Rating Scale (7), those in the placebo group worsened at 4.7 points per year compared to 3.8 in the mild urate level group (19.2% lower than placebo) and 1.7 points per year in the moderate urate level group (63.9% lower than placebo) (p < 0.001).

For the researchers, this study “provides strong evidence that long-term administration of oral inosine can be generally safe and well tolerated by early Parkinson Disease patients” and that “a disease-modifying benefit of inosine is plausible”, all of which “support a more definitive trial of inosine as a potential treatment to slow the clinical progression of Parkinson Disease.”

Source: Schwarzschild, Michael A., et al. “Inosine to increase serum and cerebrospinal fluid urate in Parkinson disease: a randomized clinical trial.” JAMA neurology 71.2 (2014): 141-150.

© 2014 American Medical Association. All rights reserved.

Posted April 12, 2016.

Greg Arnold is a Chiropractic Physician practicing in Hauppauge, NY.  You can contact Dr. Arnold directly by emailing him at PitchingDoc@msn.com or visiting his web site at www.PitchingDoc.com.

References:

  1. “About Parkinson Disease” posted on the National Parkinson Foundation Website
  2. “Ten Frequently Asked Questions About Parkinson’s Disease” posted on the Parkinson’s Disease Foundation Website
  3. Knekt P.  Serum Vitamin D and the Risk of Parkinson Disease. Archives of Neurology 2010; 67(7):808-811
  4. Gong L, Zhang QL, Zhang N, et al. Neuroprotection by urate on 6-OHDA-lesioned rat model of Parkinson’s disease: linking to Akt/GSK3β signaling pathway. J Neurochem. 2012 Dec; 123(5):876–85.
  5. Davies KJ, Sevanian A, Muakkassah-Kelly SF, et al. Uric acid-iron ion complexes. A new aspect of the antioxidant functions of uric acid. Biochem J. 1986; 235(3):747–54
  6. Cipriani S, Desjardins CA, Burdett TC, et al. Urate and its transgenic depletion modulate neuronal vulnerability in a cellular model of Parkinson’s disease. PLoS One. 2012; 7(5):e37331
  7. Parkinson Study Group SURE-PD Investigators Schwarzschild MA. Inosine to increase serum and cerebrospinal fluid urate in Parkinson disease: a randomized clinical trial. JAMA Neuro 2014 Feb;71(2):141-50. doi: 10.1001/jamaneurol.2013.5528.