Do Statins Decrease Or Increase The Risk Of Parkinson’s Disease?

Written by Dr. Steve Chaney on . Posted in Drugs and Health, Issues

The Fine Print Behind The Misleading Headline

 Author: Dr. Stephen Chaney

 Human NeuronsI hadn’t paid much attention to the headlines saying “Statin Use May Decrease Parkinson’s Risk” until the other day when I happened to glance a couple of lines below the headline and spotted a statement saying “Study Shows That Discontinuation of Statin Therapy Increases Risk of Parkinson’s”.

 I immediately said to myself “That’s bizarre. There is a total disconnect between the headlines and the study.” If you really wanted to determine whether statin use reduced the risk of Parkinson’s, you would compare the incidence of Parkinson’s disease in a group of statin users and a matched group who did not use statins.

It turns out those studies have been done, and they were inconclusive – some studies showed a slight increase in Parkinson’s in statin users, some showed a slight decrease, and most showed no correlation between statin use and Parkinson’s.

In that context, this study could equally well have been interpreted as suggesting that statin use increased the risk of Parkinson’s, but somehow none of the headlines mentioned that possibility.

Are Both Possibilities Plausible?

 Let’s look at each possibility in detail. The reasoning is complex, but let me try to walk you through it.

 Could Statins Decrease The Risk Of Parkinson’s

 Parkinson’s is caused by the progressive degeneration of the brain neurons that produce a chemical messenger called dopamine that controls muscle movement. However, the causes of nerve degeneration in Parkinson’s patients are largely unknown.

Genetics may play a small role. Environmental toxins may play a role. But most experts feel that Parkinson’s patients produce an excess of free radicals, and it is the oxidative damage caused by those free radicals that results in the loss of the ability of neurons to produce dopamine.

But even that is not the whole answer. The brain is normally able to use coenzyme Q10, which is very abundant in brain, and other antioxidants to destroy free radicals before they damage brain neurons. Somehow in Parkinson’s patients free radical production and antioxidant production have gotten out of balance.

Advocates of the theory that statins may decrease the risk of Parkinson’s, point out that statins decrease oxidative damage. So if a person was predisposed to developing Parkinson’s and oxidative damage is a major cause of Parkinson’s, it is theoretically possible that statins could slow the progression to Parkinson’s while they were taking the drug. Of course, once they stopped taking the drug the oxidative damage to dopamine-producing neurons would resume and Parkinson’s would eventually develop.

In this model- Let’s call it Model A:

1)     Oxidative damage of dopamine-producing neurons was caused by some unspecified external agent.

2)     Statins protected the neurons from oxidative damage while they were being used.

3)     Once the statin drugs were discontinued oxidative damage resumed and the risk of developing Parkinson’s increased.

This is the model favored by the authors and repeated in all of the headlines you saw.

Could Statins Increase The Risk Of Parkinson’s?

Statins also interfere with the synthesis of cholesterol and coenzyme Q10, and these are both absolutely essential for brain function. Let’s start with cholesterol:

  •  20% of the body’s membrane cholesterol is found in the myelin sheath that coats the brain’s neurons (You can think of the myelin sheath as analogous to the plastic coating that insulates an electrical wire).
  • Cholesterol can’t cross the blood-brain barrier, which means that the brain cannot utilize cholesterol from the bloodstream . It has to make its own cholesterol.

As for coenzyme Q10:

  • It is not only a powerful antioxidant. It is also absolutely essential for cellular energy production.
  • The brain has tremendous energy requirements. The brain accounts for 20% of the energy utilization of our body. Neurons burn 2 times more energy than other cells in our body.

For both of these reasons, many experts have cautioned that statin drugs have the potential to cause neurodegenerative diseases such as Parkinson’s.  In this model – Lets call it model B:

1)     The statin drugs themselves are damaging the dopamine-producing neurons by inhibiting cholesterol and coenzyme Q10 synthesis in the brain.

2)     The antioxidant effects of the statin drugs were masking the damage caused by the statins while the drugs were being used.

3)     Once the statin drugs were discontinued the underlying damage was unmasked and the patients quickly developed Parkinson’s.

What Did The Study Actually Show?

The study (Lee et al, Neurology, 81: 410-416, 2013) looked at 43,810 statin users on the island of Taiwan. The Taiwanese Health System keeps extensive records of prescription use and health conditions of everyone on the island. It also requires that statin use be discontinued as soon as the patient reach their target of < 100 mg/dL LDL cholesterol, so they had the perfect population base to study what happens when you discontinue statin therapy.

The results were:

  • The patients who discontinued statin therapy were 42% less likely to develop Parkinson’s that those who continued on statin therapy. That result is consistent with both models A & B.
  • The increased risk of developing Parkinson’s when the drug was discontinued was only seen for the statin drugs like simvastatin and atorvastatin that are able to cross the blood brain barrier. That result is actually a bit more consistent with model B (Remember that the brain has to be able to make its own cholesterol and statins block cholesterol production).
  • When the study compared people using statin drugs to those not using statin drugs there was no significant difference in the prevalence of Parkinson’s – even for those statin drugs that cross the blood brain barrier. That means that merely being on a statin drug did not influence the risk of developing Parkinson’s. It was only when patients were on statin drugs for a period of time and were subsequently taken off statins that the risk of developing Parkinson’s was affected – and the effect was to increase risk! In the context of the first two findings, that result is also a bit more consistent with model B.

The Bottom Line:

If I were writing one of those medical blogs, I would have probably have gone with the party line and told you that statins decrease your risk of developing Parkinson’s. And if I were one of those health bloggers who never let the facts get in the way of a good story, I’d probably be scaring you with headlines saying that statins increase your risk of Parkinson’s.

But, I’m a scientist. I actually read the article, and I tell it to you like it is. Here’s your bottom line.

1)     Ignore the headlines. The study they are talking about can’t distinguish between statins increasing or decreasing the risk of Parkinson’s. Don’t let anyone tell you that reducing the risk of Parkinson’s is a side benefit of statin therapy. That simply has not been proven.

2)     The study does clearly show that discontinuing the statin drugs simvastatin and atorvastatin is associated with increased risk of developing Parkinson’s. That’s a big red flag for me, because 53% of patients discontinue statin therapy because of side effects, cost or other reasons.

3)     However, statin drugs do save lives, especially for people who have already had a heart attack, so talk with your doctor about the benefits and risks of statin drugs, and which statin drugs are best for you.

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure or prevent any disease.

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Comments (8)

  • Angela

    |

    My husband has been on statins for more years than I can remember. His health has deteriorated greatly over the last 5 years and he has just been diagnosed with Parkinsons Disease. He has stopped the statins 3 weeks ago and there has been an improvement in his disposition and mental capacity. he has stopped hallucination/hearing things and and is carrying himself more balanced. He is happier in himself and not the grumpy old man he had become. He is smiling brightly. His slight tremor has now virtually disappeared. He is still very stiff. I believed it was the statins that were making him ill and now am more convinced of it than ever. It was because of what I could see that I looked for evidence on the www. There was certainly no case of ceasing the statins causing the Parkinsons.

    Reply

    • Dr. Steve Chaney

      |

      Dear Angela,
      Sometimes I am too subtle for my own good. I was raising the hypothesis that statins could cause neurological damage that increased the risk of Parkinsons, but that the neurological damage was masked by the anti-inflammatory effects of statins. Of course, once someone has been on the statins long enough it may no longer be possible to mask the symptoms. That is just a hypothesis at this point, but it would explain your husband’s situation.
      Dr. Chaney

      Reply

  • Rene Cote

    |

    After having an operation (2 stents), I received a prescription for Statins (Crestor).

    After 2 days, I started to having pain while working, back pain also, and after 5 days I could hardly walk correctly. My doctor told me I had to excercise more.
    After reading side effects on internet, I talk about it with my neighbor whose a phamacist. She told me to stop the statin treatment immediatly. After 3 days, I was back to normal.

    My father who was taking statins for 5 years was diagnosed Alzeimer. He could hardly move and was confused once in a while.
    My mother and I decided to stop my father’s statin treatment.
    After 2 weeks, my father started suddendly to walk with no help and was much much less confused. After a visit to his doctor, the Alzeimer diagnostic was removed, and replaced with a Parkinson diagnostic, because he was shajing a bit from his right hand.

    My non-scientific observation is that after being attacked by statins, their must be a period for muscles to get completly back to normal.

    I am sorry but I think you don’t follow your own recommandations: where is it proven that “statin drugs do save lives”?

    Oh yes, in studies (made by who?)

    Reply

    • Dr. Steve Chaney

      |

      Dear Rene,

      In clinical studies with patients who have already had one heart attack or otherwise have serious heart disease, statins significantly decrease the risk of a second heart attack. That has been shown in numerous clinical trials. As I pointed out, it has not been possible to prove that statins reduce heart attack risk significantly in people who have not had a heart attack. And the kind of side effects that you have described are real, and can be quite serious. This aspect of statin therapy has often been downplayed in the medical community.

      Dr. Chaney

      Reply

  • Randy Ice PT, CCS

    |

    Since oxidative stress of the dopamine producing brain cells appears to be the most likely cause of Parkinson’s, and since statins can cause or maybe protect against it, it would seem a more logical approach to prevention would be to take CoQ10 and other fat soluble antioxidants like Vitamin E and R-Alpha Lipoic Acid. This offers the best defense along with a good diet and exercise while avoiding a whole host of statin “side effects” aka unwanted direct effects, which are approaching 300 now.

    I am not convinced that statins have cardioprotective effects in secondary prevention. The original 4S study showed a 0.8%/year absolute risk reduction in the simvastatin group relative to placebo and that was in a cherry picked population of 8888 men screened from 21,000 men with prior heart attacks. So why were over 12,000 men rejected from this study.?Why was the study population so large? Because the researchers knew going in that the effects of this drug would be minimal, therefore to achieve “statistical significance” they had to rig the study with large numbers of cherry picked men. There was no difference in strokes nor MI’s in either group. Studies of women with coronary disease have shown no benefit with statins in primary ore secondary prevention.

    The absolute risk reduction in secondary prevention is so ridiculously miniscule that the long term risks of CHF, Type II diabetes, muscle and joint pain, cataracts, peripheral neuropathy, dementia, etc etc that I see in my patients very frequently make the use of these expensive drugs simply unacceptable

    This is a scam of unbelievable proportions maiming and killing millions of people around the world all in the name of “cholesterol reduction” which has no effect on atherosclerosis.

    I have directed a cardiopulmonary rehab program for the last 42 years and I see first hand the damage statins do as well as patients who have been on them for years and have another cardiac event due to progression of disease.. That is also why they have no effect on primary prevention. They Lipid Hypothesis of atherosclerosis has been dis proven and should discarded.

    Unfortunately there are $29 billion reasons why this won’t happen anytime soon.

    Reply

  • Prof A N Agrawal

    |

    I am going to stop Atorvastatin 20 which my wife , a pt of CKD on hemodialysis has been taking for last 10years and also a pt of PD on Levodopa/ carbidopa for last 3 years, and monitor the for 10-20 days whether PD symptoms improve.

    Reply

    • Dr. Steve Chaney

      |

      I always recommend checking with your physician first before going off medications. I report on clinical studies, which describe what happens for most people. However, each of us are unique and only our physicians know the pluses and minuses about changing medications for us as individuals. Tell you physician your concerns about PD and enlist their help in monitoring how your wife responds to going off or reducing Atorvastatin.

      Dr. Chaney

      Reply

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Latest Article

Should We Use Supplements For Cardiovascular Health?

Posted July 10, 2018 by Dr. Steve Chaney

Are You Just Wasting Your Money On Supplements?

Author: Dr. Stephen Chaney

 

supplements for cardiovascular health wast moneyYou’ve seen the headlines. “Recent Study Finds Vitamin and Mineral Supplements Don’t Lower Heart Disease Risk.”  You are being told that supplements are of no benefit to you. They are a waste of money. You should follow a healthy diet instead. Is all of this true?

If I were like most bloggers, I would give you a simple yes or no answer that would be only partially correct. Instead, I am going to put the study behind these headlines into perspective. I am going to give you a deeper understanding of supplementation, so you can make better choices for your health.

 Should we use supplements for cardiovascular health?

In today’s article I will give you a brief overview of the subject. Here are the topics I will cover today:

  • Is this fake news?
  • Did the study ask the right questions?
  • Is this a question of “Garbage In – Garbage Out?
  • Reducing Heart Disease Risk. What you need to know.

All these topics are covered in much more detail (with references) in my book “Slaying The Supplement Myths”, which will be published this fall.

 

How Was This Study Done?

supplements for cardiovascular healthThis study (D.J.A. Jenkins et al, Journal of the American College Of Cardiology, 71: 2540-2584, 2018 ) was a meta-analysis. Simply put, that means the authors combined the results of many previous studies into a single database to increase the statistical power of their conclusions. This study included 127 randomized control trials published between 2012 and December 2017. These were all studies that included supplementation and looked at cardiovascular end points, cancer end points or overall mortality.

Before looking at the results, it is instructive to look at the strengths and weaknesses of the study. Rather than giving you my interpretation, let me summarize what the authors said about strengths and weaknesses of their own study.

The strengths are obvious. Randomized control trials are considered the gold standard of evidence-based medicine, but they have their weaknesses. Here is what the authors said about the limitations of their study:

  • “Randomized control trials are of shorter duration, whereas longer duration studies might be required to fully capture chronic disease risk.”
  • “Dose-response data were not usually available [from the randomized control studies included in their analysis]. However, larger studies would allow the effect of dose to be assessed.”

There are some other limitations of this study, which I will point out below.

Is This Fake News?

supplements for cardiovascular health fake newsWhen I talk about “fake news” I am referring to the headlines, not to the study behind the headlines. The headlines were definitive: “Vitamin and Mineral Supplements Don’t Lower Heart Disease Risk.” However, when you read the study the reality is quite different:

  • In contrast to the negative headlines, the study reported:
    • Folic acid supplementation decreased stroke risk by 20% and overall heart disease risk by 17%.
    • B complex supplements containing folic acid, B6, and B12 decreased stroke risk by 10%.
    • That’s a big deal, but somehow the headlines forgot to mention it.
  • The supplements that had no significant effect on heart disease risk (multivitamins, vitamin D, calcium, and vitamin C) were ones that would not be expected to lower heart disease risk. There was little evidence from previous studies of decreased risk. Furthermore, there is no plausible mechanism for supposing they might decrease heart disease risk.
  • The study did not include vitamin E or omega-3 supplements, which are the ones most likely to prove effective in decreasing heart disease risk when the studies are done properly (see below).

Did The Study Ask The Right Question?

Most of the studies included in this meta-analysis were asking whether a supplement decreased heart disease risk or mortality for everyone. Simply put, the studies started with a group of generally healthy Americans and asked whether supplementation had a significant effect on disease risk for everyone in that population.

That is the wrong question. We should not expect supplementation to benefit everyone equally. Instead, we should be asking who is most likely to benefit from supplementation and design our clinical studies to test whether those people benefit from supplementation.

supplements for cardiovascular health diagramI have created the graphic on the right as a guide to help answer the question of “Who is most likely to benefit from supplementation?”. Let me summarize each of the points using folic acid as the example.

 

Poor Diet: It only makes sense that those people who are deficient in folate from foods are the most likely to benefit from folic acid supplementation. Think about it for a minute. Would you really expect people who are already getting plenty of folate from their diet to obtain additional benefits from folic acid supplementation?

The NIH estimates that around 20% of US women of childbearing age are deficient in folic acid. For other segments of our population, dietary folate insufficiency ranges from 5-10%. Yet, most studies of folic acid supplementation lump everyone together – even though 80-95% of the US population is already getting enough folate through foods, food fortification, and supplementation. It is no wonder most studies fail to find a beneficial effect of folic acid supplementation.

The authors of the meta-analysis I discussed above said that the beneficial effects of folic acid they saw might have been influenced by a very large Chinese study, because a much higher percentage of Chinese are deficient in folic acid. They went on to say that the Chinese study needed to be repeated in this country.

In fact, the US study has already been done. A large study called “The Heart Outcomes Prevention Evaluation (HOPE)” study reported that folic acid supplementation did not reduce heart disease risk in the whole population. However, when the study focused on the subgroup of subjects who were folate-deficient at the beginning of the study, folic acid supplementation significantly decreased their risk of heart attack and cardiovascular death.  This would seem to suggest using supplements for cardiovascular health is a good idea.

Increased Need: There are many factors that increase the need for certain nutrients. However, for the sake of simplicity, let’s only focus on medications. Medications that interfere with folic acid metabolism include anticonvulsants, metformin (used to treat diabetes), methotrexate and sulfasalazine (used to treat severe inflammation), birth control pills, and some diuretics. Use of these medications is not a concern when the diet is adequate. However, when you combine medication use with a folate-deficient diet, health risks are increased and supplementation with folic acid is more likely to be beneficial.

Genetic Predisposition: The best known genetic defect affecting folic acid metabolism is MTHFR. MTHFR deficiency does not mean you have a specific need for methylfolate. However, it does increase your need for folic acid. Again, this is not a concern when the diet is adequate. However, when you combine MTHFR deficiency with a folate-deficient diet, health risks are increased and supplementation with folic acid is more likely to be beneficial. I cover this topic in great detail in my upcoming book, “Slaying The Supplement Myths”. In the meantime, you might wish to view my video, “The Truth About Methyl Folate.”

Diseases: An underlying disease or predisposition to disease often increases the need for one or more nutrients that help reduce disease risk. The best examples of this are two major studies on the effect of vitamin E on heart disease risk in women. Both studies found no effect of vitamin E on heart disease risk in the whole population. However, one study reported that vitamin E reduced heart disease risk in the subgroup of women who were post-menopausal (when the risk of heart disease skyrockets). The other study found that vitamin E reduced heart attack risk in the subgroup of women who had pre-existing heart disease at the beginning of the study.

Finally, if you look at the diagram closely, you will notice a red circle in the middle. When two or three of these factors overlap, that is the “sweet spot” where supplementation is almost certain to make a difference and it may be a good idea to use supplements for cardiovascular health.

Is This A Question Of “Garbage In, Garbage Out”?

supplements for cardiovascular health garbage in outUnfortunately, most clinical studies focus on the “Does everyone benefit from supplementation question?” rather than the “Who benefits from supplementation?” question.

In addition, most clinical studies of supplementation are based on the drug model. They are studying supplementation with a single vitamin or mineral, as if it were a drug. That’s unfortunate, because vitamins and minerals work together synergistically. What we need are more studies of holistic supplementation approaches.

Until these two things change, most supplement studies are doomed to failure. They are doomed to give negative results. In addition, meta-analyses based on these faulty supplement studies will fall victim to what computer programmers refer to as “Garbage In, Garbage Out”. If the data going into the analysis is faulty, the data coming out of the study will be equally faulty. It won’t be worth the paper it is written on. If you are looking for personal guidance on supplementation, this study falls into that category.

 

Should We Use Supplements For Cardiovascular Health?

 

If you want to know whether supplements decrease heart disease risk for everyone, this meta-analysis is clear. Folic acid may decrease the risk of stroke and heart disease. A B complex supplement may decrease the risk of stroke. All the other supplements they included in their analysis did not decrease heart disease risk, but the analysis did not include vitamin E and/or omega-3s.

However, if you want to know whether supplements decrease heart disease risk for you, this study provides no guidance. It did not ask the right questions.

I would be remiss, however, if I failed to point out that we know healthy diets can decrease heart disease risk. In the words of the authors: “The recent science-based report of the U.S. Dietary Guidelines Advisory Committee, also concerned with [heart disease] risk reduction, recommended 3 dietary patterns: 1) a healthy American diet low in saturated fat, trans fat, and meat, but high in fruits and vegetables; 2) a Mediterranean diet; and 3) a vegetarian diet. These diets, with their accompanying recommendations, continue the move towards more plant-based diets…” I cover the effect of diet on heart disease risk in detail in my book, “Slaying The Food Myths”.

 

The Bottom Line

 

You have probably seen the recent headlines proclaiming: “Vitamin and Mineral Supplements Don’t Lower Heart Disease Risk.” The study behind the headlines was a meta-analysis of 127 randomized control trials looking at the effect of supplementation on heart disease risk and mortality.

  • The headlines qualify as “fake news” because:
    • The study found that folic acid decreased stroke and heart disease risk, and B vitamins decreased stroke risk. Somehow the headlines forgot to mention that.
    • The study found that multivitamins, vitamin D, calcium, and vitamin C had no effect on heart disease risk. These are nutrients that were unlikely to decrease heart disease risk to begin with.
    • The study did not include vitamin E and omega-3s. These are nutrients that are likely to decrease heart disease risk when the studies are done properly.
  • The authors of the study stated that a major weakness of their study was that that randomized control studies included in their analysis were short term, whereas longer duration studies might be required to fully capture chronic disease risk.
  • The study behind the headlines is of little use for you as an individual because it asked the wrong question.
  • Most clinical studies focus on the “Does everyone benefit from supplementation question?” That is the wrong question. Instead we need more clinical studies focused on the “Who benefits from supplementation?” question. I discuss that question in more detail in the article above.
  • In addition, most clinical studies of supplementation are based on the drug model. They are studying supplementation with a single vitamin or mineral, as if it were a drug. That’s unfortunate, because vitamins and minerals work together synergistically. What we need are more studies of holistic supplementation approaches.
  • Until these two things change, most supplement studies are doomed to failure. They are doomed to give negative results. In addition, meta-analyses based on these faulty supplement studies will fall victim to what computer programmers refer to as “Garbage In, Garbage Out”. If the data going into the analysis is faulty, the data coming out of the study will be equally faulty. It won’t be worth the paper it is written on. If you are looking for personal guidance on supplementation, this study falls into that category.
  • If you want to know whether supplements decrease heart disease risk for everyone, this study is clear. Folic acid may decrease the risk of stroke and heart disease. A B-complex supplement may decrease the risk of stroke. All the other supplements they included in their analysis did not decrease heart disease risk, but they did not include vitamin E and/or omega-3s in their analysis.
  • If you want to know whether supplements decrease heart disease risk for you, this study provides no guidance. It did not ask the right questions.
  • However, we do know that healthy, plant-based diets can decrease heart disease risk. I cover heart healthy diets in detail in my book, “Slaying The Food Myths.”

 

For more details, read the article above.

 

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure or prevent any disease.

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