March 2, 2011 -- People who regularly take the painkiller ibuprofen appear to have a modestly reduced risk of getting Parkinson’s disease, a new study shows.
For the study, which followed more than 130,000 people for six years, those who reported using ibuprofen at least twice weekly had a more than one-third reduction in the risk of getting Parkinson’s disease compared to those who didn’t take the pain reliever as often.
The researchers also pooled data from six previous studies to see if the association between ibuprofen use and Parkinson’s disease would remain. They found nearly the same reduction in risk with ibuprofen (about 30%) but not with other anti-inflammatory medications, suggesting that the effect may be specific to ibuprofen.
And the more ibuprofen a person reportedly took, the lower their risk appeared to be, something researchers call a dose-response effect.
The study analysis also showed people with 10 years or more of cumulative ibuprofen use, for example, had less than half the risk of developing Parkinson’s compared to nonusers. Those with six to eight years of use had about a 25% reduced risk.
“This suggests that ibuprofen could be, and I would like to emphasize could be, a potential neuroprotective agent,” says study researcher Xiang Gao, MD, PhD, an instructor in medicine at Harvard Medical School and an associate epidemiologist at Brigham and Women's Hospital in Boston. “Further studies are needed to replicate our finding.”
Caution Urged in Ibuprofen Use
Other experts agreed that the connection was promising but urged caution, particularly since the overall risk of developing Parkinson’s disease is low. About 1%-2% of people will develop Parkinson’s over the course of their lifetimes, and regularly taking ibuprofen or other NSAIDs over a long period may sometimes lead to side effects including stomach or kidney damage.
“It’s my opinion that we’re not ready, at all, to advise people from a public health perspective that they should start taking ibuprofen,” says James H. Bower, MD, a neurologist at the Mayo Clinic in Rochester, Minn., who wrote an editorial that accompanied the study.
“I thought their study, scientifically, was very sound. And the methodology was very good, strong, and I thought their conclusion was very reasonable,” says Bower, “so that’s not my issue.”
“Whenever in epidemiology you find an association, that does not mean causation. That’s where I’m being a little more conservative, a little more cautious,” he says.
“One explanation is the one we all want to believe, which is that ibuprofen may protect against Parkinson’s disease. That would be very exciting,” Bower says. “But unfortunately, there are other explanations that we might need to consider.”
How Ibuprofen Might Fight Parkinson’s
Other experts note, however, that a growing body of research supports the idea that ibuprofen may be uniquely protective of brain cells that produce the chemical dopamine.
Loss of those dopamine-producing neurons is thought to cause Parkinson’s, a disorder in which the brain gradually loses its ability to control the body’s movements.
People with Parkinson’s typically experience uncontrollable tremors or trembling in the jaw, face, arms or legs; stiffness; impaired coordination and balance; depression and other mood changes; skin problems; constipation; and trouble sleeping.
“The theory behind the inflammation and Parkinson’s goes back decades,” says Ali Samii, MD, associate professor of neurology at the University of Washington. “It’s biologically plausible. It’s not a very powerful protector, but it does reduce the risk.”
Samii published a study in 2009 finding that ibuprofen, but not other NSAIDs or aspirin, reduced the risk of Parkinson’s in regular users by about 25%.
“There are animal studies suggesting that the blood-barrier penetrations of NSAIDs are quite different from one another,” he says. “Ibuprofen itself may have some specific neuroprotective properties.”
In a test tube, for example, one study demonstrated that ibuprofen protected dopamine-producing nerve cells of rat brains from excessive stimulation, which can cause cell death.
For his part, Gao believes ibuprofen may work against Parkinson’s by activating a signaling pathway called the peroxisome, proliferator-activated receptor (PPAR) pathway.
“That pathway is very important for Parkinson’s disease because the PPAR pathway kind of inhibits apoptosis,” or cell death, he says. “It also plays a role in oxidative stress [and] it’s important for anti-inflammatory actions.”
Gao thinks that if scientists can discover how ibuprofen may protect brain cells, it may lead to the development of stronger and more targeted drugs that have the same effect.
“That would be a very good thing,” he says.