July 21, 2014

Cinnamon for Parkinson's? A Promising Study, a Skeptical Review

The Journal of Neuroimmune Pharmacology recently reported an interesting study finding: eating cinnamon – yes, the common spice in apple pie and gooey Danish pastries – dramatically improved the health of mice with Parkinson’s disease by reversing changes – biochemical, cellular, and anatomical – that had been brought on by the disease.

Funded by the National Institutes of Health, the study was reported in the July 9 edition of the website of Science Daily, among other outlets.
OK, I don’t get too excited about rodent studies, since they certainly won’t translate into human treatments while I’m alive. But maybe they’ll lead to breakthroughs down the road for my younger fellow PWPs.

Cinnamon.... Like Curcumin, the Wonder Compound?
This study – with its simple spice component -- reminded me a little of the amazing findings for curcumin, the active ingredient in the Indian curry spice turmeric. About 500 studies studies have shown curcumin to be effective in treating a shockingly broad array of conditions and diseases, like Alzheimer's, Parkinson's, MS, cancer, diabetes, arthritis, cardiovascular disease, and depression. It's no wonder curcumin is called “the holy powder” on the Indian subcontinent. 

Will cinnamon, in time, generate similar research-based enthusiasm? 

Kalipada Pahan, PhD -- study lead researcher and professor of neurology at Chicago’s Rush University Medical Center -- touts cinnamon's promise: "Cinnamon has been used widely as a spice throughout the world for centuries. This could potentially be one of the safest approaches to halt disease progression in Parkinson’s patients."

Pahan explained how this therapy works, at least in mice: the liver first converts the cinnamon into sodium benzoate, a substance the FDA approved in drug form as a treatment for hyperammonemia – too much ammonia in the blood. Sodium benzoate is also commonly used as a preservative in foods and beverages, because of its anti-microbial effect.

A Host of Positive Effects... on Mice
When it enters the brain – at least the brains of the PD-induced mice used in the Rush University Study – sodium benzoate seemed to serve a variety of useful purposes:
  • Stopping the loss of the proteins Parkin and DJ-1 (we know from earlier studies that PWPs have brains with decreased amounts of these two proteins),
  • Protecting brain cells,
  • Normalizing neurotrasnsmitter levels, and
  • Improving motor function in the mice with PD.

The sodium benzoate – the liver’s metabolized cinnamon -- didn’t seem to present (at least in this study) the same blood-brain-barrier issues we’ve seen with curcumin, special varieties of which have been created to overcome that barrier.

As with all promising animal studies, the big question is, “Now what?” Dr. Pahan frames it this way: “Now we need to translate this finding to the clinic and test ground cinnamon in patients with PD. If these results are replicated in PD patients, it would be a remarkable advance in the treatment of this devastating neurodegenerative disease.”

Not So Fast!
The cinnamon promise may not have the legs of the well-studied curcumin phenomenon. Last week, Harvard's "Science in the News" site weighed in on the new cinnamon details. Less hopefully than the Rush University researchers might have hoped, the article ended this way: "For now (at least where Parkinson’s disease is concerned) cinnamon still belongs in the spice rack, not the medicine cabinet."

Here's the text of that brief critical review:

A study published last month suggests that the potential value of cinnamon may go far beyond tickling our taste buds. The research group reports that cinnamon was able to substantially reverse and protect Parkinson’s disease-like symptoms in mice. Could the next groundbreaking treatment for the world’s most common neurodegenerative disease really be moonlighting as the world’s most popular baking spice? Sadly, the answer is most likely not.

Cinnamaldehyde – the chemical that gives cinnamon its famous flavor and odor – is metabolized to sodium benzoate in the liver. Sodium benzoate can enter the brain and act as an anti-oxidant. At first glance, this seems very promising! Parkinson’s disease occurs when dopamine neurons in the midbrain start to die. Scientists are not positive why the dopamine cells start dying, but a popular hypothesis is that these neurons experience high ‘oxidative stress’, which causes cells to release poisonous molecules that result in cell death. So using an anti-oxidant to reduce oxidative stress makes good sense as a potential therapy for treating Parkinson’s disease.

In fact, it makes so much sense that scientists and doctors have already been trying it for decades – unfortunately, largely to no avail. While several anti-oxidant drugs have proved tantalizingly efficacious at treating Parkinson disease-like symptoms in mice, clinical studies have found no strong evidence that they work to alleviate Parkinson’s disease in humans.

Interestingly, however, people who eat more dietary anti-oxidants (like vitamin E) throughout life may be slightly protected from developing Parkinson’s disease (although this remains an ongoing debate). It might be informative to investigate whether people or societies with especially high cinnamon intake have lower rates of Parkinson’s disease.

While this recent study presents sufficient evidence to entertain further investigation into cinnamon as a potential therapy for Parkinson’s disease, the results do not represent new or innovative insights into what is already known about anti-oxidants, oxidative stress, and Parkinson’s disease. For now (at least where Parkinson’s disease is concerned) cinnamon still belongs in the spice rack, not the medicine cabinet.

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