Hypertension May Increase Risk of Parkinson’s, Study Reports

Hypertension May Increase Risk of Parkinson’s, Study Reports

Patients with hypertension may be at a higher risk for Parkinson’s disease, according to a review of population-based studies.

The review, “Association between Hypertension and the Risk of Parkinson’s Disease: A Meta-Analysis of Analytical Studies,” appeared in the journal Neuroepidemiology.

Hypertension may cause damage in blood vessels in specific brain areas, such as the basal ganglia, which contain the substantia nigra and the striatum. In Parkinson’s, the substantia nigra experiences progressive loss of dopamine-producing neurons while the striatum has low levels of this neurotransmitter. This suggests a link between hypertension and greater prevalence of Parkinson’s.

However, previous studies have had contradictory findings, with some reporting a greater risk and others suggesting a lower risk for Parkinson’s.

To clarify this link, scientists from Qingdao University in China conducted a meta-analysis — a statistical study that combines the results of various studies — and a systematic review of the available literature.

Seven online databases were searched for literature up to July 13, 2018. From these databases, 27 observational studies were included, nine of which were population-based cohort studies (with a total of 1,230,085 participants) and 18 were case-control studies (32,121 participants). All but one study were from either North America, Europe, or Asia.

Five studies assessed hypertension by medical record, 11 through questionnaire, and two by measuring blood pressure.

In the cohort studies — prospective analyses where groups are followed to compare the risk of a specific outcome — patients with hypertension were at a significantly greater risk for Parkinson’s than participants with normal blood pressure. This was confirmed after excluding the two studies that were leading to high variability of results.

“Based on population-based cohort studies, this meta-analysis indicated hypertension might increase the risk of [Parkinson’s],” the researchers wrote.

In contrast, case-control studies — retrospective analyses where participants with or without hypertension are known from the start — suggested that hypertension might lower the risk for Parkinson’s. However, a subgroup analysis based on non-hospital records revealed no association. The variability observed in these studies was mainly due to different results in controls, depending on whether they were from hospital settings or not.

According to the team, the contradictory results in the two types of studies may have been due to a higher proportion of elderly controls with hypertension in case-control studies, particularly those conducted in the hospital setting.

Due to the link between aging and both hypertension and Parkinson’s, these studies are not suitable for exploring the risk of Parkinson’s in hypertension, the researchers said.

Among the study’s limitations, they mentioned not accounting for the use of anti-hypertensive medications as well as not being able to calculate an overall risk for Parkinson’s combining the two types of studies.

José is a science news writer with a PhD in Neuroscience from Universidade of Porto, in Portugal. He has studied Biochemistry also at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario, in London, Ontario. His work ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimer’s disease.
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José is a science news writer with a PhD in Neuroscience from Universidade of Porto, in Portugal. He has studied Biochemistry also at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario, in London, Ontario. His work ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimer’s disease.
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