Statins may reduce Parkinson's risk - study
 

Analyzing nearly 44,000 patients, scientists found that those who discontinued taking fat-soluble statins such as simvastatin (Zocor) or atorvastatin (Lipitor) were about 58 percent more likely to develop Parkinson's than those who kept taking the drugs.

Fat-soluble statins are believed to cross the blood-brain barrier, unlike water-soluble statins such as rosuvastatin (Crestor) and pravastatin (Pravachol). The drugs may decrease inflammation and even modify dopamine pathways in the brain, which are linked to Parkinson's, the study authors suggested.

http://bit.ly/15KjdXR

Lipitor clearly didn't prevent PD for me..........

I suspect that high cholesterol levels can cause/accelerate some sorts of PD (vascular PD), but protect/slow other sorts of PD (IPD).

Unfortunately, the rate of misdiagnosis/non-diagnosis is probably such that many of us have insufficient data to be able to make an informed decision.

A Medical News Today article [1], reporting the work of Pinteaux et al., states:

"Neurodegeneration was also identified in the substantia nigra six days after the mild stroke - dopaminergic neurons had been destroyed."

Huang et. al. write [2]:

"Recent studies have suggested that higher serum cholesterol may be associated with lower occurrence of Parkinson's disease (PD). ... This secondary analysis of the DATATOP trial provides preliminary evidence that higher total serum cholesterol concentrations may be associated with a modest slower clinical progression of PD."

Finally, the decision of whether to take statins has got to take into account the wider health risks, e.g, strokes.

[1] http://www.medicalnewstoday.com/articles/254301.php

[2] Huang X, Auinger P, Eberly S, Oakes D, Schwarzschild M, et al. (2011) Serum Cholesterol and the Progression of Parkinson's Disease: Results from DATATOP. PLoS ONE 6(8): e22854. doi:10.1371/journal.pone.0022854
http://www.plosone.org/article/info%...l.pone.0022854

John

The dangerous thrashing of the dying reptile
 

or, "What to do when the patent runs out on the corporate cash cow".

Our brains depend on cholesterol for building material among other things. Unless one has a family history to guide the decision, I would be very suspicious of sales reps bearing personalized coffee mugs.

There are studies out now demonstrating that statins prevent remyelination of damaged nerves. This was discovered in MS patients given high doses of Zocor to "reduce their inflammation".
Instead it caused worse damage. So now statins are no longer part of an MS protocol as a result.

In fact the high dose Zocor is no longer recommended in any humans as too toxic.
http://medicalxpress.com/news/2011-0...tin-zocor.html

All my cholesterol numbers are very "good" according to common standards (low total cholesterol, high HDL "good" cholesterol, low LDL "bad"), yet Kaiser keeps trying to push statins on me. When I asked why, they said they recommend statins for all diabetics, even if it's very well-controlled (as mine is), regardless of cholesterol numbers. It's my understanding that your response to statins can depend on your genes. 23andMe says: "...statins can cause some adverse effects, including liver problems, muscular soreness and an extremely rare condition known as rhabdomyolysis in which the muscles begin to disintegrate." Some studies show a correlation between high "good" HDL and PD. Also, some studies have actually shown increased risk of diabetes for those on statins. So I continue to refuse statins. But who knows? It's all very confusing, like everything with PD.

statins
 

I cannot believe I feel compelled to post about this subject again (am certain most readers cannot, also)--though here goes--(disclosure--I am very biased against the use of statins for anyone except middle aged men who have suffered a heart attack. and then, feel use warranted for short time during acute phase only)

From 23andme one can learn status for SLCO1B1 gene; 2 mutations have been shown to be associated with myalgias and myopathies in statin users (ONLY adverse effects studied in association with statin use and these 2 mutations--no studies for cognitive dysfunction, neuro diseases, etc). Also very high plasma statin levels--often toxic levels--for those with the mutations.
In addition, several lysosomal storage diseases have been "triggered" by statin use. Check for any alleles for these diseases. Need but one allele for statins to trigger the onset of the disease.

Note from the study by Taiwanese researchers important info:
"In Taiwan, however, the national health insurance program has requested doctors stop prescribing statins when a patient's cholesterol levels reach the treatment goal.

This Taiwanese policy, set to end on Aug. 1,
Prior research examining the link between statin use and Parkinson's disease showed inconsistent results. The new study, which took place from 2001 to 2008 on statin patients free of Parkinson's disease, also showed that participants taking water-soluble statins developed Parkinson's at about twice the rate as those taking fat-soluble statins."

Recent finding:
May 10, 2013 — The U.S. Food and Drug Administration and physicians continue to document that some patients experience fuzzy thinking and memory loss while taking statins, a class of global top-selling cholesterol-lowering drugs...
... research team has made a novel discovery in brain cells being treated with statin drugs: unusual swellings within neurons, which the team has termed the "beads-on-a-string" effect.
The team is not entirely sure why the beads form, said UA neuroscientist Linda L. Restifo, who leads the investigation. However, the team believes that further investigation of the beads will help inform why some people experience cognitive declines while taking statins.
"What we think we've found is a laboratory demonstration of a problem in the neuron that is a more severe version for what is happening in some peoples' brains when they take statins," said Restifo, a UA professor of neuroscience, neurology and cellular and molecular medicine, and principal investigator on the project.

http://www.sciencedaily.com/releases...0510150143.htm

My favorite group--Number Needed to Treat --who figure out how many people need to take a drug for X amount of time for 1 person to benefit:

Statin Drugs Given for 5 Years for Heart Disease Prevention (Without Known Heart Disease)

In Summary, for those who took the statin for 5 years:

Benefits in Percentage

98% saw no benefit
0% were helped by being saved from death
1.6% were helped by preventing a heart attack
0.4% were helped by preventing a stroke
Harms in Percentage

1.5% were harmed by developing diabetes**
10% were harmed by muscle damage

Statins Given for 5 Years for Heart Disease Prevention (With Known Heart Disease)
83 for mortality
In Summary, for those who took the statin for 5 years:

Benefits in Percentage

96% saw no benefit
1.2% were helped by being saved from death
2.6% were helped by preventing a repeat heart attack
0.8% were helped by preventing a stroke
Harms in Percentage

0.6% were harmed by developing diabetes**
10% were harmed by muscle damage
http://www.thennt.com/nnt/statins-fo...heart-disease/

Recently a 200% increase in 2 forms of breast cancer was associated with >10 yr use of statins in women ( it has never been shown that statins have any effect upon mortality or incidence of heart attacks in women)
" The reasons why the anti-cholesterol pills might stimulate cancer growth are unclear.
The researchers said one explanation may be that statins affect hormone regulation in the body, especially as the study found women on the drugs were significantly more likely to suffer cancers driven by the hormone oestrogen."


Read more: http://www.dailymail.co.uk/health/ar...#ixzz2a5TTsAMu

As per "mitochondrial dysfunction" and (problems with glucose tolerance) thought operant in PD: (admitted very small #'s of participants)

Simvastatin Effects on Skeletal Muscle
Relation to Decreased Mitochondrial Function and Glucose Intolerance
Steen Larsen, MSCI,* et al
Copenhagen, Denmark
Objectives Glucose tolerance and skeletal muscle coenzyme Q10 (Q10) content, mitochondrial density, and mitochondrial
oxidative phosphorylation (OXPHOS) capacity were measured in simvastatin-treated patients (n 10) and in
well-matched control subjects (n 9).
Background A prevalent side effect of statin therapy is muscle pain, and yet the basic mechanism behind it remains unknown. We hypothesize that a statin-induced reduction in muscle Q10 may attenuate mitochondrial OXPHOS capacity, which may be an underlying mechanism.
Methods Plasma glucose and insulin concentrations were measured during an oral glucose tolerance test. Mitochondrial
OXPHOS capacity was measured...and Q10 content was determined.

Conclusions These simvastatin-treated patients were glucose intolerant. A decreased Q10 content was accompanied by a decreased maximal OXPHOS capacity in the simvastatin-treated patients. It is plausible that this finding partly explains the muscle pain and exercise intolerance that many patients experience with their statin treatment.
(J Am Coll Cardiol 2013;61:44–53) © 2013 by the American College of Cardiology Foundation

Dr Huang noted findings from the very long running Honolulu men study in which low LDL cholesterol was associated with increased incidence of Parkinson's

Mov Disord. 2008 May 15;23(7):1013-8. doi: 10.1002/mds.22013.
Low LDL cholesterol and increased risk of Parkinson's disease: prospective results from Honolulu-Asia Aging Study.
Huang X, Abbott RD, Petrovitch H, Mailman RB, Ross GW.

I will note that the study referenced in the first posting is an observational study. Not a great vehicle for basing questionable therapies upon.