Statins May Protect Against Parkinson's Disease
Patients who continued taking simvastatin and atorvastatin had significantly reduced risk of developing Parkinson's disease compared with those who discontinued statin therapy.
Patients who continued taking simvastatin and atorvastatin had significantly reduced risk of developing Parkinson’s disease compared with those who discontinued statin therapy.
In addition to lowering cholesterol levels, statins may also help to protect patients against Parkinson’s disease, according to a study published online on July 24, 2013, in Neurology.
Prompted by evidence showing statins have anti-inflammatory effects, the researchers set out to evaluate the effect of statin therapy on Parkinson’s disease incidence. By using data from Taiwan, where the national health insurance policy requests that physicians end statin therapy once patients reach their cholesterol goals, the researchers were able to compare the frequency of Parkinson’s disease in patients who discontinued statin use with its frequency in patients who continued the therapy.
The study included 43,810 patients aged 50 and older who began statin therapy between 2001 and 2008 and who did not have a history of Parkinson’s disease. Every person-day during the study period was classified as statin use or nonuse, and discontinuation of therapy was identified if a patient did not receive a medication refill. Parkinson’s disease was determined by hospital discharge diagnosis or outpatient diagnosis of the disease made by a neurologist.
The results indicated that the incidence rate of Parkinson’s disease was 1.68 per 1 million person-days for patients taking lipophilic statins and 3.52 per 1 million person-days for patients on hydrophilic statins. After adjusting for age, sex, comorbidities, and other medication use, continuation of lipophilic statin therapy was associated with a decreased risk of Parkinson’s disease when compared with patients who discontinued therapy.
Simvastatin and atorvastatin use was associated with a significantly reduced risk of Parkinson’s (hazard ratio of 0.23 and 0.33, respectively, compared with statin discontinuation), and a trend toward decreased risk was observed with lovastatin and fluvastatin use. The protective effects of simvastatin and atorvastatin use were particularly pronounced in women (hazard ratio of 0.11 and 0.24, respectively), and the benefits of atorvastatin use were also evident in patients older than 65 (hazard ratio of 0.42). These protective effects were not observed in association with use of hydrophilic statins.
The researchers note that lipophilic statins may be better able to protect against Parkinson’s disease because they are able to cross the blood-brain barrier more easily than hydrophilic statins. “These good penetration abilities into the neuronal and glial cells could be associated with more antioxidant and anti-inflammatory effects than the hydrophilic statins,” the researchers write.
The results also indicated that lipophilic statin users had a decreased risk of death compared with those who discontinued statin use (hazard ratio of 0.32). Only a trend toward decreased death was observed in continuing hydrophilic statin users.
The researchers suggest that further study is needed to investigate the relationship between long-term lipophilic statin use and Parkinson’s disease incidence as well as the potential differences in risk associated with sex and age.
In an accompanying editorial, Eng-King Tan, MD, and Louis C.S. Tan, MD, agree that more research is needed to evaluate the potential effects of statins, but note that the current study adds to a growing body of evidence suggesting that statins have neuroprotective benefits. “For those who have to be on statins, it is a comforting thought that there is a potential added advantage of having a lower risk of [Parkinson’s disease], and possibly other neurologic disorders as well,” the editorialists write.