Is the long term use of statins associated with lower risk for Parkinson’s?

Original article: Poly TN, Islam MM, Walther BA, Yang HC, Nguyen PA, Huang CW, Shabbir SA, Li YJ. November 16, 2017. Exploring the Association between Statin Use and the Risk of Parkinson’s Disease: A Meta-Analysis of Observational Studies. Neuroepidemiology, 49, 142-151.

The takeaway

Statins are drugs known for their cholesterol-lowering effects and prescribed for the prevention of cardiovascular disease. Over the last decade, statins have also been shown to have additional biochemical effects on neurodegeneration in Parkinson’s. This study pooled data from 13 existing studies and found that overall, long term statin use is associated with lower risk for Parkinson’s. Further research is necessary to discover whether the lower Parkinson’s risk seen in those people on statin treatment is actually caused by the statins themselves, or another underlying, but as yet unidentified, common factor.

Why is it important?

Statins are among the most commonly prescribed drugs in developed countries. It is important to know whether these drugs alter the risk for Parkinson’s. Several published studies had shown that statins reduce risk, but others had found that they increased it.

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IMPACT

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Impact Opinion

This large meta-analysis brings some clarity to a controversial area; that is, whether statins lower risk of Parkinson’s. While the results suggest they do, one has to remember that lower disease risk does not necessarily mean that the drug will slow progression in someone who already have developed Parkinson’s.

Background

Unlike clinical trials, observational studies can be thought of as snapshots of information on available data. Usually, these data refer to health patterns or drug treatments, for large numbers of individuals. Several such studies have been performed to answer the question of whether people receiving statins are at higher or lower risk of developing Parkinson’s, given increasing evidence that the biochemical effects of statins extend to promoting neuronal survival and reducing inflammation. But these studies revealed a mixed picture: some reported higher risk while others reported lower risk in those on statins.

The details

In a bid to settle this open question, studies published over the last decade were selected if they met three criteria: 1) were published in English, 2) had included people receiving statins and had focused on whether they had a Parkinson’s diagnosis and 3) contained adequate statistical information on risk.

Combining 13 studies effectively pooled 4,877,059 study subjects, 24,596 of whom also had Parkinson’s.

The overall pooled reduction in Parkinson’s was 30% for those on statins for more than 3 years compared to those who were not on these drugs. This estimate differed depending on the geographical region in which the different studies were conducted: studies in people from Asia reported greater reduction (38%) for those on statins, compared to those from N America (31%) and Europe (14%). A subanalysis indicated that the type of statin was also important: whereas simvastatin and atorvastatin were associated with lower risk, pravastatin was associated with elevated risk.

Observational studies cannot be used to establish whether the lower risk for Parkinson’s found in those people on statins is actually caused by these drugs or whether another underlying cause is driving both of these effects.

Next steps

Clinical trials are necessary To establish whether statins have the potential to modify disease progression in Parkinson’s.

Related work

Carroll CB, Wyse RKH (2017) Simvastatin as a Potential Disease-Modifying Therapy for Patients with Parkinson’s Disease: Rationale for Clinical Trial, and Current Progress. J Parkinson’s Disease, 7, 545-568.

PD-STAT website

Original article: Poly TN, Islam MM, Walther BA, Yang HC, Nguyen PA, Huang CW, Shabbir SA, Li YJ. November 16, 2017. Exploring the Association between Statin Use and the Risk of Parkinson’s Disease: A Meta-Analysis of Observational Studies. Neuroepidemiology, 49, 142-151.
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