Does anyone know someone who developed Parkinson's after taking Lipitor?

To make a long story short... my father started taking Lipitor during 2004 and took the drug for about a year and a half until he started incurring strange side effects. He developed Parkinson's symptoms shortly after quitting the drug and has been struggling with the disease ever since. He is still mobile but he is getting worse every day.

I have been reading online that lots of people have developed neurodegenerative diseases after taking Lipitor and other statins. I have also read that a large scale study (involving 16,000 people) of a possible link between statins and neurodegenerative diseases is being conducted but I haven't been able to find out much more.

Does anyone here know someone who developed Parkinson's after taking Lipitor or other statins?

the two facts may be unconnected. I don't mean to insult your worry and pain, but this is a very widely used drug and there are going to be anecdotes about people taking it and having other things happen. For example, a lot of middle-aged men who take Lipitor develop male pattern baldness. Keep doing your research, but read every claim with a critical eye.

...but the fact that a large scale independent study on a possible connection is underway has me thinking that reports of people developing neurodegenerative diseases after taking statins are not isolated cases.

Edit: I almost forgot... thanks for the kind words.

Of course they are taking a statin because they have high cholesterol which is thought to contribute to coronary artery disease and people with coronary artery disease often have AMI's.

David

study rather than a final pronouncement. In this case, are the statins ineffective in preventing heart attack? Are they increasing the risk? Is the model of high cholesterol causing heart attack accurate?

My fasting tri-glycerides have ranged from 368 to 1280 before I started taking Tricor. Now they are about 150. I don't anyone would argue it's good to have the equivalent of 30 weight motor oil running through your blood vessels.

David

and eating oatmeal every am for 5 yrs now. Statin industry is as enormous as viagra. Now pharmaceutical funded study says they should give it to children!

On a hunch, I googled statin dopamine (dysregulation of dopamines being involved in Parkinsonism).

Here is a very recent report that I found on statins & dopamine in rats:

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1576073

Br J Pharmacol. 2005 April; 144(7): 933–939.
Published online 2005 February 14. doi: 10.1038/sj.bjp.0706106.

PMCID: PMC1576073
Copyright 2005, Nature Publishing Group
High doses of simvastatin upregulate dopamine D1 and D2 receptor expression in the rat prefrontal cortex: possible involvement of endothelial nitric oxide synthase

* This study aims to investigate whether or not long-term statin treatment causes upregulation of D1 and D2 receptor gene expression with concomitant increase in endothelial nitric oxide synthase (eNOS) expression in Sprague–Dawley rats.
* Serum triglyceride levels were dose dependently reduced in the simvastatin-treated rats reaching statistical significance at the highest dose (49% reduction), while pravastatin caused similar effects (52%) at the same dose. Cholesterol levels remained unchanged in both groups at all doses.
* Simvastatin, 10 or 30 mg kg−1 day−1, increased D1 and D2 receptor expressions in the prefrontal cortex. Similar upregulation was observed neither with simvastatin in the striatum nor with pravastatin in both brain regions.
* Simvastatin (10 mg kg−1 day−1) also increased eNOS expression in the prefrontal cortex but not neuronal NOS or inducible NOS.
* D1 receptor activation by chloro-APB (5 μM) increased cAMP levels in synaptosomes prepared from the prefrontal cortex of control and simvastatin-treated rats by 88 and 285%, respectively. This effect was markedly attenuated by the selective D1 antagonist SCH-23390 (25 μM).
* D2 receptor activation by quinpirole (5 μM) had no effect on the basal cAMP levels in synaptosomes prepared from the prefrontal cortex of control and simvastatin-treated rats, while the same concentration of quinpirole completely abolished the D1 receptor-mediated increase.
* These results suggest that lipophilic statins can alter dopaminergic functions in the prefrontal cortex possibly via a central mechanism. The possibility of a nitric oxide mechanism involving eNOS requires further investigation.

http://www.medicalnewstoday.com/articles/60876.php



What became of the 2007 study? Is it ongoing? Has it been concluded?

NEUROLOGY 2008;70:1418-1422
© 2008 American Academy of Neurology
Statin use and the risk of Parkinson disease
Angelika D. Wahner, PhD, Jeff M. Bronstein, MD, PhD, Yvette M. Bordelon, MD, PhD and Beate Ritz, MD, PhD

From the Department of Epidemiology (A.D.W., B.R.), UCLA School of Public Health; and the Department of Neurology (J.M.B., Y.M.B.), David Geffen School of Medicine at UCLA and the Greater Los Angeles Veterans Administration Medical Center, Los Angeles, CA.

Address correspondence and reprint requests to Dr. Angelika D. Wahner, UCLA School of Public Health, Box 951772, 650 Charles E. Young Drive, Los Angeles, CA 90095-1772

Objective: To investigate associations between statin (3-hxydroxy-3-methylglutaryl-coenzyme A reductase inhibitor) use and Parkinson disease (PD).

Methods: We used a population-based design to recruit 312 incident idiopathic PD cases and 342 controls from three rural California counties.

Results: We observed a higher frequency of statin use among controls vs cases (OR 0.45; 95% CI 0.29 to 0.71) and a strong dose-response relation. The strongest protective association between statin use and PD was observed in long-term (≥5 years) users (OR 0.37; 95% CI 0.18 to 0.78). There was no difference by gender or age. We noted 60 to 70% risk reductions for each individual statin except pravastatin.

Conclusion: Ascribing causality to these associations is premature and further studies are needed to confirm a potential neuroprotective role for statins in PD.

GLOSSARY: B-D test = Breslow-Day test; NO = nitric oxide; PD = Parkinson disease; PEG = Parkinson's Environment and Genes.

"However, it should be noted that significant adverse events relating to the CNS has not been reported after long-term use of statins in humans (Pedersen et al., 1996)."

and you'll have to wait for the results, I have nothing to add about whether the risks are higher or not.

The problem with this stuff is that Lipitor is being taken by an older population and one most likely to develop diseases like Parkinson's. That means the group will have to be very large to see any increased risk from taking statins and that will mean the study will take some time to complete.

My own feeling is that statins aren't nearly as benign as they were originally thought to be and they've been handed out far too liberally to people who really didn't need them. That's just me, though. They are proven lifesavers in people with genetically determined high lipid levels.

The good news about Parkinson's is that it can be treated for some years, the symptoms alleviated. Better news is that stem cell therapy has been very promising in rebuilding the area of the brain that is destroyed by Parkinson's.

However he happened to develop the disease, your dad has some hope out there.

I think it was Lipitor. He is having a terrible time.

Crestor, which is a statin as well:

http://www.spacedoc.net/crestor.htm


snip

We have now learned much more about the side effects of Crestor. We have learned that cognitive, muscle and nerve problems, due to the inevitable impairment of glial cell cholesterol synthesis and mevalonate blockade are only part of the problem. The Crestor side effect potential, that it shares with all other statins, is far more basic than this. Now we have learned that mitochondria are an inevitable target of statins. Because of inhibition of CoQ10 availability with its powerful anti-oxidant effect, mitochondria are left fully exposed to the mutagenic effect of free radicals. The resulting mutations of mitochondria are what is causing the legions of permanent, disabling side effects.

snip

Permanent neuropathy, permanent myopathy, chronic neuromuscular degeneration, and Parkinsonism and ALS-like cases now are thought by some to be the result of permanent statin-induced, mitochondrial damage. Furthermore, the inherent ability of the body to identify and correct the daily load of mutations is impaired because of the previously unrecognized effect of dolichol inhibition from the earlier mevalonate blockade. If this is beginning to sound like a domino effect, you are right. We still are seeing the dominos topple one by one as time goes by - the result of marketing a class of drugs before it was fully investigated.

I refused after reading about the side effects. She is very upset with me, but I am not taking that risk.

My husband and also a physician who's wife I met on the internet. She told me of a study they had translated from Germany that provides link to Lipitor. Will share this thread with her. Lipitor has decided to include CoQ10 as it depletes it in body. (Tell your father to start taking it right away. Husband takes 1000mg.) The fact that Lipitor is now concluding it must put in supplement is indicative of their guilt re Parkinsons imo.

...he is not taking Lipitor?

so lipitor would exacerbate problem. Husband takes incredible amt of supplements...after 5 yrs he remains off big parkinsons drug but that may change. Keep your Dad moving. T'ai Chi is recommended and walking sideways and backwards builds new brain pathways. Also if he's having problem walking... tell him to take a great big step and say NO!! Supposedly that makes brain take another pathway. Dancing to his favorite music is great as well. I subscribe to daily google alerts along with friends and family networking for any help they can find. pm me anytime ;-) am certain there will be enormous class action suits re statins some day in the future.