Strokes and Parkinsons

Dear colleagues, I am Christoph Diener from the University of Essen in Germany. For the month of November, I have identified four interesting studies in neurology.

The first one was published in the European Heart Journal, and it addresses the question of whether, if you treat atrial fibrillation with anticoagulation, you can prevent the development of dementia.^[1] There are a number of studies which basically show that people with atrial fibrillation have an increased risk for dementia, and this is true for both Alzheimer disease and vascular dementia.

Investigators from Sweden looked at the national health registry and the drug prescription registry. They identified 444,106 patients who had atrial fibrillation. About half of them were anticoagulated and the other ones were not anticoagulated, for whatever reason. They found that in a period between 2006 and 2014, the risk of developing dementia was reduced by almost 30% in patients who were anticoagulated. This was true both for warfarin and for NOACs [novel oral anticoagulants]. This would indicate in a large sample of almost 450,000 patients with atrial fibrillation that anticoagulation can prevent the development of dementia.

The next study deals with secondary stroke prevention and smoking.^[2] This was a study which investigated pioglitazone in patients who had a TIA [transient ischemic attack] or stroke over a period of 5 years. This was called the IRIS trial. The investigators looked at patients who at baseline had the event—stroke or TIA—and smoked; then they looked at patients who quit smoking in the next 5 years. This percentage at the beginning was about 30%, and 42% of these patients stopped smoking. What they observed was a risk reduction of 35% for a recurrent stroke, myocardial infarction, and vascular death if people stopped smoking. The benefit was very clear for stroke and death. It was not significant for myocardial infarction.

Now, I would like to move to Parkinson's disease. There are a number of epidemiologic studies which would indicate that the consumption of caffeine can reduce the risk for Parkinson's disease. A publication in Neurologyinvestigated whether caffeine given twice daily in a dose of 200 mg in a period of between 6 and 18 months has an impact on the symptoms of Parkinson's disease.^[3]

They randomized 120 patients to either caffeine twice daily or to placebo. The study could not show a benefit on the neurologic symptoms of Parkinson's disease, and there were no cognitive testing results in patients on caffeine. What the study does not answer is whether caffeine has a preventive effect on the cause of Parkinson's disease.

The last study was published in Annals of Neurology and investigated whether traumatic brain injury is a predictor of Parkinson's disease.^[4] The investigators identified almost 89,000 patients who had Parkinson's disease and 118,000 controls around the age of 65 years. They looked at the connection between traumatic brain injury in the past 5 years to the incidence of Parkinson's disease. They found that there was a 64% increase in the risk of developing Parkinson's disease if the traumatic brain injury was within the past 5 years. The risk increased with a shortening of the time interval between traumatic brain injury and Parkinson's disease.

Now, whether there is a causal relationship or whether the traumatic brain injury happened due to falls—because the patients already started having motor symptoms of Parkinson's disease—cannot be answered by this study. It also has no impact on patient handling because you cannot prevent traumatic brain injury or falls to prevent Parkinson's disease. At least it is an interesting study, indicating that head trauma and brain trauma might be risk factors for Parkinson's disease.

Ladies and gentlemen, here are two studies from the stroke field and two interesting studies from the Parkinson's disease field. I'm Christoph Diener, a neurologist from the Department of Neurology in Essen, Germany. Thank you for listening.

• References

Medscape Neurology © 2017  WebMD, LLC 

Any views expressed above are the author's own and do not necessarily reflect the views of WebMD or Medscape.

Cite this article: Four New Updates in Stroke and Parkinson Disease - Medscape - Dec 06, 2017.

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Exercise not drugs!

When Jillian Carson was diagnosed with Parkinson's disease at the age of 49, the medical specialists had little to offer her in the way of treatment.

"They tell you that you have this neurodegenerative disease that there's no cure for, but if you take this little pill you'll be good for about 10 years," she told On the Island host Gregor Craigie.

"And then you decline," she said. "You start to decline and then basically there's no hope." 

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Carson is now chair of the Parkinson's Wellness Project which is preparing to open a stand-alone centre in Victoria with the help of an anonymous donation of $500,000.

Isolating effect 

Carson said Parkinson's has an isolating effect, where sufferers tend to retreat into their homes and inactivity.

"If you put someone with Parkinson's in a chair, they'll be gone in five years," she said.

"If I can get people out of their houses they'll keep coming." 

The Parkinson's Wellness Centre, to be located in a midtown Victoria strip mall next to a doughnut shop, will offer rigorous exercise programs, including boxing.

After her own diagnosis Carson, who had worked as a physiotherapist, studied research-based Parkinson's wellness recovery exercise programs in the United States.

While there is no cure for Parkinson's disease Carson said rigorous exercise programs, including boxing, can slow the progress of the degenerative disorder. (Bill Peterson)

"The latest research on Parkinson's disease is that exercise actually slows the progression of the disease. And the sooner you get doing Parkinson's specific exercises, the better," she said.

Carson said to achieve the release of natural dopamine in the body — the chemical lacking in Parkinson's patients — sufferers have to, "exercise harder than you think you could ever do in your life."

Coaches are needed because people with Parkinson's can't accurately adjust the speed or intensity of their movements. 

"We may be thinking we're going really fast but we're going really slow," she said. "We don't have the sensory feedback in our bodies."

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Statins and Parkinsons

The researchers in this Penn State study analyzed data from a database of over 50 million people, 22,000 of whom had Parkinson’s disease. Of that sample, they reduced it to 2,322 patients with new diagnoses of Parkinson’s. Then, they paired each person within the sample size to another individual without Parkinson’s, and those people made up the control group.

Researchers then established which patients had been taking Statins and how long they’d been taking them for before they developed Parkinson’s symptoms. Their findings suggested that prior Statin use resulted in a higher risk of Parkinson’s and, interestingly enough, “was more noticeable during the start of the drug use.”

“Statin use was associated with higher, not lower, Parkinson’s disease risk, and the association was more noticeable for lipophilic statins, an observation inconsistent with the current hypothesis that these statins protect nerve cells,” explained one of the researchers, Xuemei Huang, Ph.D.. “In addition, this association was most robust for use of statins less than two-and-a-half years, suggesting that statins may facilitate the onset of Parkinson’s disease.”

Other Health Issues Related to Statins 

It’s not just Parkinson’s that relates to Statins, either. These drugs can have a whirlwind of side effects and increase one’s risk of developing a number of different diseases. Since Statins block the body’s production of CoQ10, taking Statins can result in fatal muscle inflammation as well as congestive heart failure (which is ironic given that many heart disease patients take them).

Another study published in Expert Review of Clinical Pharmacology revealed that, despite Statin drugs being marketed for their ability to decrease the artery disease called atherosclerosis, they may actually stimulate it and cause heart failure.

Another study published in the American Journal of Physiology found that some of the effects of Statins advance the process of aging, and pointed out that long term use of Statins have been associated with several adverse health effects including myopathy (skeletal muscle weakness), neurological issues, and an increased risk of diabetes.

The researchers stated: “In addition, considering their possible side effects, long-term adherence to statin treatment poses a potential risk, especially among individuals without cardiovascular disease. The primary use of statins should be critically assessed, especially when considering the potential risks associated with statin use.”

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Teaching brains new patterns

Exactly what triggers dystonia — an involuntary muscle contraction of the hand, fingers, neck or mouth, which is sometimes very painful — is unclear. But some researchers think the underlying problem that causes it may also be the key to treating it, and other brain-linked disorders like Parkinson's.

Ajax, Ont. guitarist Jamie Shear suffers from dystonia, a movement disorder that is more common among musicians than any other professional group. (Facebook)

Ajax, Ont. professional musician Jamie Shear explained how he first noticed his own dystonia.

"Picked up the guitar. Couldn't hold the pick the way I wanted to," he said. "So I went to see a doctor."

Shear's doctor is Robert Chen, a dystonia specialist at Toronto Western Hospital. Chen diagnosed Jamie with "focal dystonia," a type of involuntary contraction involving just one or a few muscles.

The Dystonia Medical Research Foundation says the disorder affects 300,000 people in the U.S. and Canada. According to the U.K.-based Dystonia Society, it can affect members of any profession which requires repeated movements — like writers, athletes or craftspeople — but is more common among musicians than any other professional group.

The underlying problem in all cases is normal brain plasticity — the brain's ability to form new connections between neurons through experience — gone rogue.

• The Nature of Things: Changing Your Mind
• The National: The Learning Brain

"Say someone would keep practicing a musical instrument," said Chen. "You want to induce a good type of plasticity, to learn how to play maybe a very difficult sequence. But in some cases this can go wrong and lead to an unfavourable or abnormal type of motor program."

Muscle function is initiated by the motor cortex, straddling the top of your brain. Towards the bottom, the basal ganglia make motions smooth. Right behind, the cerebellum acts as an autopilot, monitoring your body position on the fly, calculating how best to move when the motor cortex says "go."

"Traditionally, we think that dystonia is mainly a disturbance of the basal ganglia," said Chen. "Patients with a stroke in the basal ganglia will often develop dystonia. But in the last, I'd say, five to 10 years, there is lots more evidence that the cerebellum is also involved."

'Tangled networks' lead to disorder

Philippe Isope, of France's Institute of Cellular and Integrative Neurosciences, studies the cerebellum in his lab in Strasbourg, France. ​He explains that neuronal circuits are like a highway system that constantly monitors and adjusts itself — plastically.

"Imagine that you have a big mesh of highway," Isope said. "If the action is okay, there is a mechanism that will say, 'That was a good road.' Communication points between two cells — between two neurons — will be strengthened by the fact that the action is well done."

Sometimes, though, networks get tangled up, and muscles stiffen. The result is Shear's fingers lifting away from his guitar pick, for example, or a person with torticollis — excruciating neck spasms.

Dystonia can also affect the eyes, eyelids, mouth, tongue and rectum.

"This problem is a communication breakdown," said Isope. 

The solution may be to use the brain's plasticity to stop the rogue neural loop, and restore the good one.

Teaching the brain new patterns

"Basically, what you do is to provoke new plasticity in the network, and then the network can learn again the correct pattern, in a sense."

Back in Ajax, Shear's dystonia has not gone away. Researchers are studying ways to help brain circuits get over their hiccups.

"I have gone and volunteered for different areas of experimentation, where they've created headaches for me," he said. "But enough for them to do research and give me free Botox at the same time."

Botox injections weaken the tiny muscles that make Jamie's digits lift from his pick. His cerebellum should respond by backing off these muscles, and assigning others in their place. The same approach may work for the tens of thousands of other Canadians with focal dystonia.

Having learned how to replace hiccupping neural circuits in people with dystonia, the next step could be to restore motor function in stroke patients, for example — where some circuits have died, but others can be recruited; or getting Parkinson's patients to sing in choirs, thereby restoring facial expression.

How best to promote brain plasticity in different clinical situations is the big question.

The research goes on.

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Treating Parkinsons

Increased risk of PD

In the UK, researchers found an almost double risk between statin use and this debilitating illness. 

That research was done over the course of two decades and involved close to 16,000 people!

Dr. Kailash Chand, who is deputy chairman of the British Medical Association, commented that the dangers of taking statins are “far greater than any potential benefits,” and that their use should be restricted.

And now, researchers from the Penn State College of Medicine have come out with their own findings. This study crunched the data on over 30 million patients, also concluding that those on statin drugs have an increased risk of Parkinson’s.

So why is it that a few years ago, a group of researchers tried to make us believe that statins somehow protect against Parkinson’s?! At the time, one Big Pharma-connected doctor wrote that he found it a “comforting thought” that statins have this extra advantage of lowering the risk of Parkinson’s.

Why, that flies in the face of every single thing we know about cholesterol and the brain. And the only ones being comforted here are the drugmakers who are raking in the billions on meds like Lipitor, Crestor and Zocor.

You see, as one British expert said, Mother Nature made cholesterol for a reason. Cholesterol protects your brain! And when you artificially drive it down to basement levels, you subject yourself to all kinds of neurological diseases. On top of that, the Penn researchers noted that statins block not only cholesterol, but also CoQ10, an enzyme that’s “essential for cell function.”

That’s about the worst-kept secret in medicine. The very well-documented depletion of CoQ10 is so big that a public interest group recently attempted to get the FDA to add a black-box warning to these drugs, alerting users to take a CoQ10 supplement along with a statin.

And last year I told you about a study (one that got almost no coverage in the mainstream media), showing how statins can increase plaque buildup in your arteries and both cause and worsen heart failure.

Any way you look at it, statins are bad news. And unbelievably just one of these drugs, Lipitor, brings in $7 billion a year!

It’s time to stop the insanity!

If your doctor keeps giving you the “cholesterol talk,” and pushing you to start up on one of these drugs, maybe your best (and safest) course of action is to find another doctor.

“Statin use linked to increased Parkinson’s risk”, 

Nancy A. Melville, October 26, 2016, Medscape, medscape.com

Our results provide additional evidence regarding the lower incidence of PD among statin users.

Background: Recent studies have suggested a relation between statin use and the risk of Parkinson’s disease (PD). However, the conclusions are inconsistent. Some studies found an increased incidence of PD among statin users; others found a decreased incidence. Others showed that PD incidence was related to baseline cholesterol levels. 

Objectives: To examine the association between baseline levels of low-density lipoprotein cholesterol (LDL-C), long-term statin use, and the incidence of PD. 

Methods: The study group consisted of a historical cohort of 94,308 men and women in Israel aged 45 years or more without PD or statin use at baseline, between 2000 and 2007. PD incidence among long-term statin users was compared with that among nonusers. The cohort was divided into 4 groups according to baseline LDL-C levels, and their relative risks of developing PD were  calculated with adjustment for potential confounders (sex, age, socioeconomic status, history of ischemic heart disease, hypertension, stroke, and smoking). The association between different variables was analyzed with a Cox proportional hazards model. 

Results: During the study period, 1035 incident cases of PD were identified. Statin use was associated with a significant decrease in the incidence of PD (odds ratio, 0.73, 95% confidence interval, 0.60-0.88; P = .001). 

No association was found between baseline LDL-C levels and PD risk. 

Conclusions: Our results provide additional evidence regarding the lower incidence of PD among statin users. These findings warrant further research regarding the possible neuroprotective role of statins in PD and other neurodegenerative diseases.

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Parkinsons and statins

TUESDAY, June 20, 2017 (HealthDay News) -- People on cholesterol-lowering statins may have a slightly increased risk of developing Parkinson's disease, a new study suggests.

Researchers said the finding doesn't prove statins are to blame. But, they added, the findings undercut the notion that statins might help protect against Parkinson's.

Where does that idea come from? Past research has shown that people with high cholesterol tend to have a lower risk of Parkinson's, explained Dr. Xuemei Huang, a professor of neurology at Penn State College of Medicine.

Since many of those people are treated with statins, that led to speculation that the drugs -- rather than high cholesterol itself -- might be protective.

But so far, studies have come to mixed conclusions, according to Huang. Some have tied statins to a lower Parkinson's risk, while others have found either no connection or an increased risk.

Enter the new study. Using medical records from over 4,600 U.S. adults -- with and without Parkinson's -- Huang's team found that statin users had a higher risk of being diagnosed with the neurological disease.

When the researchers dug deeper, they found that certain statins -- those that are fat-soluble, rather than water-soluble -- were tied to Parkinson's risk.

That's notable, according to Huang, because only fat-soluble statins can cross from the blood into the brain. Fat-soluble statins include drugs such as atorvastatin (Lipitor), fluvastatin (Lescol) and simvastatin (Zocor).

"This doesn't mean that statins are causing Parkinson's," Huang noted.

She stressed that people who are taking the drugs to cut their risk of heart attack and stroke should not stop.

But, Huang said, the findings raise an important question: Could some statins hasten the progression of someone who is in the early, symptom-free stages of Parkinson's?

The study uncovered hints that could be the case, according to Huang. People on statins faced an increased risk of a Parkinson's diagnosis within 2.5 years of starting the drugs, but those odds dipped thereafter.

A neurologist who was not involved in the study said the connection between statins and Parkinson's has been controversial.

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Statin Use Linked to Increased Parkinson's Risk

New findings from a large national claims database show the use of cholesterol-lowering statin drugs to be associated with an increased risk for Parkinson's disease (PD), contrary to previous research suggesting the drugs have a protective effect for PD.

"We identified 20,000 Parkinson's disease patients and looked at whether using statins was associated with a higher or lower risk, and we found people using statins have a higher risk of the disease, so this is the opposite of what has been hypothesized," senior author Xuemei Huang, MD, PhD, vice chair for research at Penn State College of Medicine, Hershey, Pennsylvania, told Medscape Medical News.

While high cholesterol has been shown to have a protective effect on the risk for PD, the role of statin use has been the subject of debate.

Among studies supporting a benefits was research published in 2012 in the Archives of Neurology showing a "modest Parkinson's disease reduction" with the use of statins.

In looking at the issue in a previous study of their own, Dr Huang and colleagues in fact found an increased risk associated with statin use, and they sought in the new study to further explore the association in a much larger cohort.

For the new study, presented here at the American Neurological Association (ANA) 2016 Annual Meeting, the researchers turned to data from the MarketScan Commercial Claims and Encounters database, including information on 30,343,035 persons aged 40 to 65 years between January 1, 2008, and December 31, 2012.

Of the subjects, 21,559 were identified as having PD on the basis of criteria of having a primary or secondary diagnosis, using anti-Parkinson's medication, or having deep-brain stimulation surgery.

In the cross-sectional analysis, the use of cholesterol-lowering drugs, including statins or nonstatins, was associated with a significantly higher prevalence of Parkinson's disease (odds ratio [OR], 1.61 - 1.67; P < .0001) after adjustment for age, sex, and other comorbidities, such as hyperlipidemia, diabetes, hypertension, and coronary artery disease.

For a comparative neurodegenerative group, the researchers also looked at the association of statin with diagnosis of Alzheimer's disease but found only a minimal association (OR, 1.01 - 1.12; P = .055).

The associations of cholesterol-lowering medications with PD were strongest among patients with hyperlipidemia, and there were no significant differences between lipophilic or hydrophilic statins, as well as the other nonstatin cholesterol-lowering drugs, in their effect on PD risk.

"We know that overall weight of the literature favors that higher cholesterol is associated with beneficial outcomes in Parkinson's disease, so it's possible that statins take away that protection by treating the high cholesterol," Dr Huang explained.

"Another possibility is that statins can block not only the cholesterol synthesis but also synthesis of coenzyme Q10 that is essential for cell function."

The researchers also stratified persons according to how long they had been receiving treatment by using a lagged matched case-control analysis of 2458 pairs of PD cases and controls.

In the cross-sectional analysis, both statins and nonstatin cholesterol-lowering drugs were associated with PD, but in the lagged case-control analysis of treatment duration, only statins remained significantly associated with PD risk.

The highest risk was linked to the earlier period after starting statins (OR, 1.93 for less than 1 year of use; 1.83 for 1 to 2.5 years; and 1.37 for 2.5 years or more; P trend < .0001).

"The increased risk of Parkinson's is more likely when statins are first used, so we think it could be that the statins 'unmasked' Parkinson's," Dr. Huang said. "Namely, people may be already on the way to Parkinson's and when they use statins to control the high cholesterol, it gives Parkinson's a push to reveal its clinical symptoms.

"Based on this data, we think caution should be taken before advancing statins to be protective of Parkinson's disease," she added. "The data are not clear yet."

A meta-analysis published earlier this year in the journal Pharmacoepidemiology and Drug Safety suggests that one reason for the inconsistencies in evidence of the role of statins is that many studies fail to adjust for cholesterol levels.

In that report, studies that did not make the adjustment showed a protective effect of statins (relative risk, 0.75), but those that did adjust for cholesterol or hyperlipidemia showed no protective effect: Those adjusting for hyperlipidemia had a relative risk of 0.91, and for cholesterol, the relative risk was 1.04.

"The apparent protective effect of statins on risk of Parkinson's disease is at least partially explained by confounding by statin indication," the authors said.

In addition, a separate meta-analysis published in the Journal of Neurology in 2013 suggested that there is a significant publication bias in recent literature toward reporting protective effects of statins in PD.

"The current study is one of very few studies reporting potential negative effects of statin in Parkinson's disease," Dr Huang noted.

The study was funded by grants from the National Institutes of Health, Pennsylvania State University College of Medicine-Milton S. Hershey Medical Center, General Clinical Research Center (GCRC), GCRC Construction, and the Center for Applied Studies in Health Economics. The authors have disclosed no relevant financial relationships.

American Neurological Association (ANA) 2016 Annual Meeting. Abstract S137. Presented October 16, 2016.

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Use of statins and the risk of Parkinson's disease: a retrospective case-control study in the UK.

Abstract

BACKGROUND:

Case reports have related the use of HMG-CoA reductase inhibitors ('statins') to Parkinson's disease (PD). Paradoxically, however, statins may have potentially beneficial effects on neurodegenerative diseases due to their anti-inflammatory properties

OBJECTIVE:

To explore the risk of the development of PD in association with untreated hyperlipidaemia and with hyperlipidaemia treated with lipid-lowering drugs in the UK primary care setting.

METHODS:

We conducted a case-control analysis using the UK-based General Practice Research Database (GPRD). Cases were incident PD cases > or =40 years of age between 1994 and 2005. One control was matched to each PD case based on age, sex, general practice and index date. Lipid-lowering drug use was assessed by exposure timing (current vs past use) and by exposure duration (1-9, 10-29 or > or =30 prescriptions) prior to the index date for both cases and controls. Odds ratios (OR) were calculated using conditional logistic regression, adjusted for body mass index, smoking and various cardiovascular, metabolic and psychiatric co-morbidities.

RESULTS:

We identified 3637 cases with an incident idiopathic PD diagnosis, and the same number of controls. Compared with patients without hyperlipidaemia, those with untreated hyperlipidaemia did not have an altered relative PD risk (adjusted OR 0.98, 95% CI 0.74, 1.30). The adjusted ORs for current use of > or =30 prescriptions for statins or fibrates compared with non-use of statins or fibrates were 1.06 (95% CI 0.75, 1.51) and 1.25 (95% CI 0.51, 3.06), respectively.

CONCLUSIONS:

In this observational study, the long-term use of statins or fibrates was not associated with a substantially altered relative risk of developing PD.

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A prospective study of statin use and risk of Parkinson disease

Statins have been found to have potent anti-inflammatory and immunomodulating effects, which led to the hypothesis that statins could be neuroprotective agents. However, the beneficial effects of statins could be offset by their unfavorable effects on lowering plasma coenzyme Q10 and urate. We therefore prospectively examined whether use of statins was associated with altered risk of PD.

Conclusions

We found that regular use of statins was associated with a modest reduction in PD risk. The possibility that some statins may reduce PD risk deserves further consideration.

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Statins, plasma cholesterol, and risk of Parkinson's disease: A prospective study

Previous findings on the association of statins, plasma lipids, and Parkinson's disease (PD) are confounded by the fact that statins also affect lipid profiles. 

We prospectively examined plasma lipids and statin use in relation to PD in the Atherosclerosis Risk in Communities (ARIC) Study. 

Statin use and plasma lipids were assessed at baseline (visit 1, 1987-89) and at three triennial visits thereafter (visits 2-4) until 1998. 

Potential PD cases were identified from multiple sources and validated where possible. The primary analysis was limited to incident PD cases diagnosed between 1998 and 2008. Odds ratios and 95% confidence intervals were derived from multivariate logistic regression models. Statin use was rare at baseline (0.57%) but increased to 11.2% at visit 4. 

During this time frame, total-cholesterol levels decreased, particularly among statin users. Fifty-six PD cases were identified after 1998. Statin use before 1998 was associated with significantly higher PD risk after 1998 (odds ratio = 2.39, 95% confidence interval 1.11-5.13) after adjusting for total cholesterol and other confounders. 

Conversely, higher total cholesterol was associated with lower risk for PD after adjustment for statin usage and confounders. 

Compared with the lowest tertile of average total cholesterol, the odds ratios for PD were 0.56 (0.30-1.04) for the second and 0.43 (0.22-0.87) for the third tertile (Ptrend = 0.02). 

Statin use may be associated with a higher PD risk, whereas higher total cholesterol may be associated with lower risk. 

These data are inconsistent with the hypothesis that statins are protective against PD. © 2015 International Parkinson and Movement Disorder Society

http://onlinelibrary.wiley.com/doi/10.1002/mds.26152/abstract

Parkinsons and statins

Patients who are susceptible to developing Parkinson’s disease may speed up the onset by taking prescribed statins, according to a new study.

There is a lot of debate around the side effects of the anti-cholesterol drugs, which approximately eight million people in the UK take every single day.

But new research from Penn State College of Medicine warns that people should be more cautious about taking the medicine if they have family history of dementia.

This is not to say that statins cause Parkinson’s, but that they may aggravate an underlying risk. 

Xuemei Huang, Professor of Neurology, said: “We are not saying that statins cause Parkinson’s disease, but rather that our study suggests that statins should not be used based on the idea that they will protect against Parkinson’s.”

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Statins and Parkinsons

New findings from a large national claims database show the use of cholesterol-lowering statin drugs to be associated with an increased risk for Parkinson's disease (PD), contrary to previous research suggesting the drugs have a protective effect for PD.

"We identified 20,000 Parkinson's disease patients and looked at whether using statins was associated with a higher or lower risk, and we found people using statins have a higher risk of the disease, so this is the opposite of what has been hypothesized," senior author Xuemei Huang, MD, PhD, vice chair for research at Penn State College of Medicine, Hershey, Pennsylvania, told Medscape Medical News.

While high cholesterol has been shown to have a protective effect on the risk for PD, the role of statin use has been the subject of debate.

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Statins and Parkinsons

A new large study presented at the American Neurological Association Annual Meeting has found a strong connection between cholesterol-lowering medications and Parkinson’s disease. Contradicting previous claims that statins are protective against PD.

In recent years there has been a considerable effort to try to find new applications for statins. Reports have tried to link statins with positive results on a wide range of conditions, such as: Alzheimer’s, Parkinson’s, Cancer, Multiple Sclerosis and Depression.  

These claims have been somewhat surprising considering that the brain and nervous system have the highest requirements for cholesterol and low cholesterol levels are associated with cognition problems, increased suicide, and an increased risk for some types of cancer. Many people have suspected that the data is being carefully cherry picked in an attempt to show a false benefit and expand the use of statins into other areas.

In the new study, researchers analysed data from the MarketScan Commercial Claims and Encounters database - including information on 30,343,035 persons aged 40 to 65 years. The use of cholesterol-lowering drugs was associated with a significantly higher prevalence of Parkinson's disease.

This is not the first time that we have seen an absence of the predicted benefits of statins in real life data. For example, a large study in 2011 collected data from 289 of 290 municipalities in Sweden and found that the predicted benefits of statins had not materialised, despite a dramatic increase in statin use.

An important finding of this new study is that all of the cholesterol lowering drugs included were associated with an increased risk of PD. Suggesting that the harms of the drugs could be directly related to the cholesterol-lowering effect. This adds to the mountain of data that now exists to show that having a low level of cholesterol is worse than having a high level.

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