Discontinuing statins may increase Parkinson’s risk

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People who stop taking their lipophilic statins may be at higher risk for developing Parkinson disease (PD) compared with patients who continue their lipid-lowering regimen, according to population-based research from Taiwan.

Using information in Taiwan’s National Health Insurance Research Database, researchers identified 43,810 people who did not have PD and who initiated statin therapy between 2001 and 2008. The drugs included in the study were simvastatin (Zocor, Merck), fluvastatin (Lescol, Novartis), lovastatin (Mevacor, Merck), atoravastatin (Lipitor, Pfizer), pravastatin (Pravachol, Bristol Myers Squibb) and rosuvastatin (Crestor, AstraZeneca).

Taiwan’s National Health Insurance Reimbursement Policy requests physicians to stop patients’ statin therapy once low-density-lipoprotein cholesterol levels are less than 100 mg/dL.

“This policy allowed us to see whether there was any difference in the risk of Parkinson’s in people who stopped taking statins compared to the ones who kept taking them,” study author Jou-Wei Lin, MD, PhD, of National Taiwan University, said in a press release.

The study, published in the July 24 online edition of Neurology, found that continued use of lipophilic statins was associated with a decreased risk of PD with an adjusted hazard ratio of 0.42.

The effect was especially pronounced for simvastatin and atorvastatin and was more evident among women and the elderly. 

However, there was no protective effect observed among users of hydrophilic statins.

Further analysis of PD incidence rate revealed a higher risk of with continued hydrophilic statin use. The incidence rate for PD was 1.68 per million person-days for lipophilic statins vs. 3.52 per million person-days for hydrophilic statins.

The authors speculated that the ability of lipophilic statins to get into the brain could offer some benefit to regular users.

“These good penetration abilities into the neuronal and glial cells could be associated with more antioxidant and anti-inflammatory effects than the hydrophilic statins,” they wrote.

In an accompanying editorial, Eng-King Tan, MD, and Louis C.S. Tan, MD, of Singapore General Hospital noted that there could be other physiologic mechanisms at work.

“While there is some consensus that lipophilic statins can easily cross the blood-brain barrier and are likely to have a direct neuroprotective effect, the possibility of an indirect effect through changes in cholesterol or other lipids cannot be discounted,” they wrote.

Since the study authors were not able to assess participants’ cholesterol and lipid levels, the editorial writers continued, it is possible that high cholesterol levels that necessitated continued statin treatment could have contributed to PD risk.

Lin and his colleagues acknowledged there could have been an effect caused by an intermingling of factors, including cholesterol and lipid levels as well as certain PD risk factors.