Cinnamon May Help Treat Parkinson's Disease
Cinnamon is likely not the first thing that comes to mind when discussing treatment options for Parkinson’s disease. However, if the findings of a new mouse study bear out, clinicians may one day use the popular spice to help manage this neurological disease.
Parkinson’s disease is a progressive nervous system disorder that affects motor function. Signs and symptoms include hand tremors, muscle rigidity (that can be painful), slowed or halting speech, difficulty writing, loss of automatic movements (e.g., swinging your arms while walking, gesturing), difficulty with gait and walking, balance problems, and impaired posture.
Cinnamon and Parkinson's Disease
Two primary forms of cinnamon available in the United States are Chinese cinnamon (Cinnamonum cassia) and Ceylon cinnamon (Cinnamonum verum). Chinese cinnamon, which comes from the bark of evergreen trees in Indonesia, is somewhat hotter and has a stronger taste than its Ceylon cousin, which is harvested from evergreen trees in Sri Lanka. In the laboratory, scientists have noted some other differences.
In the new study, which was conducted by a team at Rush University Medical Center and headed by Kalipada Pahan, PhD, the researchers examined both types of cinnamon using mass spectrometric analysis. According to Pahan, “Ceylon cinnamon is much more pure than Chinese cinnamon as the latter contains coumarin, a hepatotoxic [harmful to the liver] molecule.”
Also of interest is the fact that cinnamon is metabolized by the body into sodium benzoate. You may recognize this substance as a food additive/preservative, which has antimicrobial effects. It also is an approved drug (by the Food and Drug Administration, FDA) for metabolic defects of the liver associated with high levels of ammonia (hyperammonemia), which can be deadly. (Just because sodium benzoate has been approved by the FDA, however, does not mean everyone believes this substance is safe, as noted in this article on the preservative.)
The authors built on previous research in which they explored how sodium benzoate is involved in Parkinson’s disease. They noted, for example, that sodium benzoate is capable of stopping the loss of two proteins—DJ-1 and Parkin--that are essential for maintaining normal neurotransmitter levels in the brain.
Dopamine is a neurotransmitter that plays a critical role in Parkinson’s disease. When the dopamine-producing nerve cells die, as they do in people who have Parkinson’s disease, individuals experience symptoms of the disease.
In this study, the investigators found that ground cinnamon given to mice with Parkinson’s disease metabolized into sodium benzoate and stopped the loss of DJ-1 and Parkin. Therefore, cinnamon shows potential as a treatment to help stop progression of Parkinson’s disease.
Will cinnamon work in people who have Parkinson’s disease? Hopefully that question will be answered with further research that involves giving cinnamon to humans who have the disease.
Since scientists don’t know what causes Parkinson’s disease, the quest for effective treatment options has been a challenge. Among the factors that may have a role in causing the disease are exposure to various common chemicals and genetic factors. Treatment options have relied mainly on drugs to help relieve symptoms as well as deep brain stimulation for more serious cases.
The introduction of a natural treatment option such as cinnamon could be an important breakthrough for Parkinson’s disease patients. However, much more research is necessary before anyone can recommend using cinnamon as a treatment option for Parkinson’s disease.
Khasnavis S, Pahan K. Cinnamon treatment upregulates neuroprotective proteins Parkin and DJ-1 and protects dopaminergic neurons in a mouse model of Parkinson’s disease. Journal of Neuroimmune Pharmacology 2014; DOI:10.1007/s11481-014-9552-2
Khasnavis S, Pahan K. Sodium benzoate, a metabolite of cinnamon and a food additive, upregulates neuroprotective Parkinson disease protein DJ-1 in astrocytes and neurons. Journal of Neuroimmune Pharmacology 2012 Jun; 7(2): 424-35