[Stitcher]

Low cholesterol levels linked with higher risk of Parkinson's disease
· Fears that statins could cause increase in illness
· Health charities urge caution over findings

Polly Curtis, health correspondent
Monday January 15, 2007
The Guardian, United Kingdom
http://www.guardian.co.uk/frontpage/...990648,00.html

Scientists are to investigate why people with low cholesterol levels appear to be more likely to develop Parkinson's disease, following concerns that statins - given to control cholesterol - could cause an increase in the numbers of people with the illness.

About 2.3 million adults in the UK take statins to help control their cholesterol levels; the American scientists have found that those with lower levels of cholesterol are more likely to develop the degenerative neurological disorder of Parkinson's disease.

The link between statins and Parkinson's is not yet understood, and health charities last night urged caution. But the scientists behind the research warn that if they get confirmation of the finding, in their follow-up study of 16,000 people, there could be a surge in Parkinson's diagnoses in the next five years as the effects of the drug set in.

The initial study compared 124 people diagnosed with Parkinson's with a control group of 112. They found that the people with low levels of "bad" LDL cholesterol were in excess of three times more likely to be in the Parkinson's group than those with high cholesterol.

But they also found that those in the trial who took statins were less likely to develop Parkinson's disease, though the study's leader suggested this could be because the group with Parkinson's had had low cholesterol all their lives and that the effect of low cholesterol could be cumulative.

Statins are the world's biggest selling drug. The drug company Pfizer reported sales of $12.2bn (£6.2bn) for its statin, Lipitor, in 2005. The National Institute for Clinical Excellence last year recommended more people take them in the UK, raising the number of customers from 2.3 million to 5.2 million.

The head of the study, Xuemei Huang, at the University of North Carolina, said: "I'm definitely concerned [about the initial findings] which is why I'm conducting a prospective study of 16,000 people."

People should not stop taking statins, she said. The risk of heart disease in those who should be taking statins far outweighed the risk of developing Parkinson's.

The study, which is reported today in the journal Chemistry and Industry, has raised more questions than it has answered. It has not, for example, established whether low cholesterol is a cause or consequence of Parkinson's.

David Dexter, senior lecturer in neuropharmacology at Imperial College London, said: "Although the association is worrying, the study was carried out only in a small number of subjects and hence needs confirming in a larger population. Lower LDL-C levels may also be a consequence of Parkinson's and not a cause. Indeed, the study did not take into account the dietary intake of the two groups in the study, [which] may be important since some Parkinson's patients find it difficult to eat or even swallow food, thus reducing the intake of fats."

Dr Huang said the well-established link between Parkinson's and apoE2, a gene associated with lower LDL cholesterol, supported her theory that low LDL was the culprit in many cases of Parkinson's.

Kieran Breen, director of research at the Parkinson's Disease Society, said people should be wary of such a small study. "Further research into any link between low LDL cholesterol and cholesterol-lowering drugs with Parkinson's is needed. We hope that the proposed study will shed further light on this. The exact causes of Parkinson's are unknown. Research is ongoing. It is generally understood that Parkinson's [arises] from genetic and environmental factors."

Peter Weissberg, medical director of the British Heart Foundation, said: "We are concerned that any suggestion of a link between statins and Parkinson's disease would unnecessarily scare the millions of people benefiting from statins in the UK. There is no evidence to suggest that statins cause [the] disease. On the other hand, there is overwhelming evidence that statins save lives by preventing heart attacks and strokes."

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'Link' Between Statins and Parkinson's Probed

Posted on: Monday, 15 January 2007, 12:00 CST
http://www.redorbit.com/news/health/...ource=r_health

EXPERTS sought to reassure patients after scientists announced they were planning an in-depth study on the link between statins and Parkinson's disease. The cholesterol-lowering drugs are taken by an estimated three million Britons and are renowned for preventing heart attacks and strokes. But now scientists are planning a detailed study after research showed a link to Parkinson's disease, which affects about 120,000 people in the UK. Charities urged people to continue taking their statins, saying the drugs saved lives. According to a report in the magazine Chemistry & Industry, researchers in the United States are planning a largescale clinical trial on the link. It comes after experts, led by Xuemei Huang from the University of North Carolina, said they had found the strongest link yet between low-density lipoprotein (LDL) cholesterol levels and Parkinson's. High levels of LDL cholesterol are linked to heart disease. Statins are known to reduce these LDL levels. The study of 124 patients revealed that those with low levels of LDL cholesterol were about three times as likely to develop Parkinson's disease as those with higher levels. Study leader Dr Xuemei Huang told the magazine she was worried by the results. "Yes I am very concerned, which is why I am planning a 16,000-patient prospective study to examine the possible role of statins, " she said.She said there could be big surges in the number of Parkinson's cases in the next five years if a link is confirmed.British experts sought to calm fears, saying there was little or no evidence of a link.Dr David Dexter, senior lecturer in neuropharmacology at Imperial College, London, said: "With the evidence we have at the moment, I would say there is not much cause for concern that statin use may cause Parkinson's disease. "The study by Huang and colleagues indicating an association between lower LDL levels and Parkinson's disease goes against current scientific beliefs."

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[Stitcher]

Lipitor, Neuromuscular Degeneration, and Recovery

Page Expires: Monday, January 22, 2007 12:44:24 AM
Modified: Monday, November 13, 2006 7:33:57 PM
http://www.cqs.com/lipitor.htm

Numerous adverse side effect reports have implicated Lipitor and other statin drugs as a probable cause for severe neuromuscular degeneration. Some people who have been using Lipitor for as little as two months report serious muscle weakness and pain. Some who have taken it longer report much more serious symptoms, similar to Muscular Dystrophy, Parkinson's Disease, Multiple Sclerosis or ALS - Lou Gehrig's Disease - in which they are losing neuromuscular control of their bodies or losing significant muscle mass. Others have reported serious liver and kidney damage. Still others have been told that they have nvCJD, the human equivalent of mad cow disease.

For instance, in an article entitled "Life After Lipitor" that appeared in the newspaper Tahoe World on January 27, 2004, Tahoe City (California) resident Doug Peterson began having serious neuromuscular problems after taking Lipitor for two years. He began losing muscular coordination and slurring words when he spoke. Then he lost balance, followed by loss of fine motor skills - he had difficulty writing. He went from doctor to doctor, trying to figure out what could be happening. Finally one doctor suggested that he stop taking Lipitor, and the downward health spiral slowed, but the damage had been done. The drug had apparently triggered cerebellar ataxia, a degenerative disease that causes deterioration of the cerebellum.

These adverse effects have begun appearing in peer-reviewed medical journals, and numerous people have reported similar symptoms at public adverse effect reporting websites such as medications.com. People have reported "trouble swallowing, trouble talking and enunciating words, feeling fatigued all the time, neck aches," "motor neuropathy which mimics ALS," "Blinding headaches, nausea, vertigo, disorientation, memory loss, extremely dry eyes, pain and stiffness in my neck and calf muscles, abominal pain," and "Muscle pain, weakness, spasms, buzzing in right leg. Can't hold arms or head up in vertical position for 2 minutes without extreme pain and weakness."
How could Lipitor potentially cause this kind of harm to so many different parts of the body? Lipitor is a "statin" drug which inhibits the production of cholesterol in order to lower LDL cholesterol counts. By limiting the production of cholesterol, Lipitor may be causing membrane degeneration in neural and muscle tissue.

The problem is this: cholesterol is essential in your body for many functions. It forms part of what is called the cell membrane - the semi-permeable outer layer of every cell in your body. It also helps transport the major components of the cell membrane, called "phospholipids," that are made from essential fatty acids (EFAs). Without enough cholesterol we would die, because our tissues are constantly being repaired and replaced with new cells.

Our body produces several thousand milligrams of cholesterol per day to carry out these essential functions, and each day the excess of cholesterol is supposed to be naturally recycled. If your body doesn't have enough new cholesterol each day, you cannot repair and replace your cell membranes and they will eventually degenerate.

The continual recycling of cholesterol happens naturally when you have sufficient ascorbate, another name for vitamin C. Excess cholesterol is naturally converted to bile acid and then excreted. But if you don't consume enough vitamin C (about 2000-3000 milligrams per day for an adult), cholesterol builds up in your bloodstream. It is here that doctors make a critical error: instead of telling you to take more vitamin C to recycle cholesterol naturally, they prescribe Lipitor, which may create a deficiency of new cholesterol.

Lipitor also blocks the production of an essential micronutrient called Co-Q10, necessary to maintain heart muscle health, and has no effect on lipoprotein(a), the actual sticky protein that constitutes heart disease "plaques." So instead of preventing heart disease, Lipitor may be increasing heart disease risk.

If Lipitor and other similar statin drugs are in fact causing neural and muscular cell degeneration by over-restricting the production of cholesterol, this is a very serious matter indeed. There are almost twenty million people in the U.S. on Lipitor alone, and probably millions more on other statin drugs (Zocor, Pravachol, Mevacor, Altocor, Lescol, Crestor, etc.). Many millions more are now having statin drugs recommended to them by their doctors. Are they all going to become victims of cell membrane degeneration and nervous system problems?

There are few long-term studies that bear out the safety of these drugs. Pfizer, the manufacturer of Lipitor, has acknowledged on their public website that side effects such as "muscle pain or weakness" could be a "sign of serious side effects," and has even put a name on the condition - rhabdomyolysis - previously a rare disease usually only caused by traumatic injury - but these are classified as a reason for people to stop the medication rather than an indication that the drug should be withdrawn or banned.

Dr. Duane Graveline, scientist, family doctor, and former astronaut for NASA, wrote a book called "Lipitor, Thief of Memory" (now out of print) and is updating it along with its title to "Statins - Side Effects and the Misguided War on Cholesterol." His book will soon be available.

His website is http://www.spacedoc.net/statin_side_effects.html.

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Statins, cholesterol, Co-enzyme Q10, and Parkinson's disease.

Parkinsonism Relat Disord. 2005 Mar;11(2):81-4.
Lieberman A, Lyons K, Levine J, Myerburg R.
Department of Neurology, University of Miami School of Medicine, Miami, FL 33136, USA. al@parkinson.org
http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract

'Statins', drugs that lower cholesterol are widely used. Statins block cholesterol in the body and brain by inhibiting HMG-Co-A reductase. This pathway is shared by CoQ-10. An unintended consequence of the statins is lowering of CoQ-10. As CoQ-10 may play a role in PD, its possible statins may worsen PD. Such a report has appeared. Statins came into wide use in 1997-1998, 6 years before our study began. Thus 74% of our patients on a statin had a PD duration of 1-6 years versus 56% of our patients not on a statin. A direct comparison of patients on a statin and not on a statin would bias the study in favor of the statins: patients on a statin would have a shorter disease duration and less advanced PD. Therefore we divided the patients into two groups. Group I consisted of 128 patients on a statin, and 252 not on a statin who had PD for 1-6 years. In this group, disease severity (Hoehn & Yahr Stage), levodopa dose, Co-enzyme Q10 use, prevalence of 'wearing off', dyskinesia and dementia were similar. Group II consisted of 45 patients on a statin and 200 patients not on a statin who had PD for 7-22 years. In this group disease severity, levodopa dose, Co-enzyme Q10 use, prevalence of wearing off, dyskinesia and dementia were similar. Statins although they may affect Co-enzyme Q10 levels in the body and the brain, do not worsen PD at least as assessed by stage, and prevalence of wearing-off, dyskinesia, and dementia.

PMID: 15734664 [PubMed - indexed for MEDLINE]

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[Stitcher]

Doctors Pre-Empt Study By Dismissing Link Between Parkinson's and Statins

Source: Herald, The; Glasgow (UK)
By DAMIEN HENDERSON
Posted on: Monday, 15 January 2007, 12:00 CST
http://www.redorbit.com/news/health/...ource=r_health

WHILE scientists are preparing an in-depth study of the link between Parkinson's disease and statins, some eminent medics are pre- empting the results and have dismissed the suggestion.

Some three million Britons use statins, the cholesterollowering drug used to prevent heart attacks and strokes.

Researchers in America are planning a large-scale clinical trial on the link after experts, led by Xuemei Huang from the University of North Carolina, said they had found the strongest link yet between Low-density Lipoprotein (LDL) cholesterol levels and Parkinson's.

Experts sought to reassure patients over the safety of the drugs yesterday, insisting they saved lives and had not been shown to cause Parkinson's, which affects around 120,000 people in the UK.

The study in America of 124 patients revealed that those with low levels of LDL cholesterol were around three times as likely to develop Parkinson's disease as those with higher levels.

The cause of Parkinson's is unknown, but is thought to be due to a combination of genetic and environmental factors.

DrXuemei Huang, who led the study, told Chemistry & Industry magazine: "I am very concerned, which is why I am planning a 16,000- patient prospective study to examine the possible role of statins, " she said.

Scotland, which has the highest death rate from coronary heart disease in the UK, is also believed to have a higher proportion of patients taking the drug, with the use of statins having doubled in the last five years.

Dr David Dexter, senior lecturer in neuropharmacology at Imperial College, London, said: "With the evidence we have at the moment, I would say there is not much cause for concern that statin use may cause Parkinson's disease.

"Indeed, previous studies have demonstrated that statins can increase brain dopamine concentration, the chemical transmitter deficient in Parkinson's."

Dr Kieran Breen, director of research and development at the Parkinson's Disease Society, said: "A study comparing such small numbers of people with Parkinson's and those without cannot establish low LDL cholesterol as a cause of Parkinson's. We should be wary of drawing any firm conclusions from this research."

Professor Peter Weissberg, medical director of the British Heart Foundation, said: "We are concerned that any suggestion of a link between statins and Parkinson's disease would unnecessarily scare the millions of people benefiting from statins in the UK."

He added that while there was no evidence to suggest that statins caused Parkinson's disease, there was overwhelming evidence they prevented heart attacks and strokes.

"Nobody should stop taking statins on the basis of this report. If they do, they will be putting themselves at increased risk, " he said.

Dr Patricia Limousin, consultant neurologist at University College London, said: "There is no evidence that statin drugs cause Parkinson's disease. In fact, these drugs were related to a lower occurrence of Parkinson's disease in Huang's study."

[reverett123]

...especially if you take l dopa...

1: Neurochem Int. 2006 Apr;48(5):404-14. Epub 2006 Jan 26.

Postmortem brain fatty acid profile of levodopa-treated Parkinson disease
patients and parkinsonian monkeys.

Julien C, Berthiaume L, Hadj-Tahar A, Rajput AH, Bedard PJ, Di Paolo T, Julien
P, Calon F.

Molecular Endocrinology and Oncology Research Centre, Centre Hospitalier de
l'Universite Laval Research Centre (CHUL), Que., Canada.

Fatty acids play a critical role in brain function but their specific role in
the pathophysiology of Parkinson disease (PD) and levodopa-induced motor
complications is still unknown. From a therapeutic standpoint, it is important
to determine the relation between brain fatty acids and PD because the brain
fatty acid content depends on nutritional intake, a readily manipulable
environmental factor. Here, we report a postmortem analysis of fatty acid
profile by gas chromatography in the brain cortex of human patients (12 PD
patients and nine Controls) as well as in the brain cortex of monkeys (four
controls, five drug-naive MPTP monkeys and seven levodopa-treated MPTP monkeys).
Brain fatty acid profile of cerebral cortex tissue was similar between PD
patients and Controls and was not correlated with age of death, delay to autopsy
or brain pH. Levodopa administration in MPTP monkeys increased arachidonic acid
content (+7%; P < 0 .05) but decreased docosahexaenoic acid concentration (-15%;
P < 0.05) and total n-3:n-6 polyunsaturated fatty acids ratio (-27%; P < 0.01)
compared to drug-naive MPTP animals. Interestingly, PD patients who experienced
motor complications to levodopa had higher arachidonic acid concentrations in
the cortex compared to Controls (+13.6%; P < 0.05) and to levodopa-treated PD
patients devoid of motor complications (+14.4%; P < 0.05). Furthermore, PD
patients who took an above-median cumulative dose of levodopa had a higher
relative amount of saturated fatty acids but lower monounsaturated fatty acids
in their brain cortex (P < 0.01). These results suggest that changes in brain
fatty acid relative concentrations are associated with levodopa treatment in PD
patients and in a non-human primate model of parkinsonism.

PMID: 16442670 [PubMed - indexed for MEDLINE]

[olsen]

Ben A. Barres and Stephen J Smith. Science, November, 2001, Vol 294, pp1296-7.
"The smooth operation of the nervous system depends on rapid commmunication between nerve cells at meeting areas called syapses. Although synapses were first identified 100 years ago, their fomation, a process called synaptogenesis, has remained something of a mystery....two intriguing but unanticipated conclusions about synaptogenesis have been reached. The first is that neurons by themselves form few synapses unless they have help from other nerve cells called glial cells(1-3). The second reported by Mauch, et. al..., is that the synapse-promoting signal released by glial cells is CHOLESTEROL(emphasis mine)...

...Neurons in culture form few synapses unless glial cells called astrocytes are present. Astrocytes increase synapse number by secreting cholesterol bound to large lipoprotein particles containing apolipoprotein E (apoE).

These particles are internalized by neurons, leading to increased cholesterol within neuronal membranes . It is possible that apoE also activates yet to be identified signaling pathways within the neurons . These changes stimulate an increase in the number and efficacy of synapses."

Refs noted in above quote:
1. FW Pfrieger. BS Barres, Science 277. 1684 (1997)
2. EM Ullian., S Sapperstein, et al Science 291, 65 (2001)
3. K. Nagler, D. Mauch, j Physiol533. 665 (2001)
4. DH Mauch, et al Science 294. 1354 (2001)

[as an aside --apoE IS the SAME lipoprotein that researchers "target" by statin use in patients with alzheimer's--statins decrease apoE, which many researchers "theorized" was responsible for amyloid aggregation found in Alzheimer's--and because individuals with APOE-4 gene variations have been shown more susceptible to developing Alzheimer's in a couple of studies...what if their theory is incorrect??]

It may or may not be important that the lipid that constitutes the largest percentage of all fats found in the SUBSTANTIA NIGRA is "dolichol" and dolichol production is directly dependent upon the mavelonate pathway--the same pathway that is totally blocked by all statins. does this fact have clinical relevance--who knows--no one has asked the question. it is just assumed that it must be okay..or hoped that it is in fact not an issue. or by not addressing it, it is in fact a non issue....

[olsen]

Carolyn, if I had your abilities, the citizen's petition to the FDA I have been researching and writing over the past year to implore them to conduct phase 4 studies on lipitor to determine if there exists a causal relationship between lipitor and parkinson's would have been completed by now. thank you for finding these articles and posting them....
I know i am repeating myself, but the study by Lieberman has a few problems from my analysis--though the most IMPORTANT part (my opinion)in this study was the notation that 5 patients who were originally in the non-statin group were started on a statin during the trial.
ALL FIVE OF THE SUBJECTS DEVELOPED WORSENING OF THEIR SYMPTOMS AFTER STARTING THE STATIN.

the statins were stopped for a "washing out" period--and after 2 weeks when the symptoms did not revert to pre-statin levels the investigators decided that these effects were not caused by the statin and the drugs were reordered......

statins do more than just decrease LDL (which is not a fat, but a lipid and a protein that act as carriers for cholesterol and triglycerides)

statins interrupt isoprentylation of many substances one of which results in a depression in selenoprotein expression. the functions of selenium are carried out by selenoproteins. several selenoproteins are expressed in the brain. glutathione peroxidase is one of these, serving an important role as protection from reactive oxygen species-induced cell damage. selenium concentrations in the CSF and serum of patients with PD are lower compared to normal subjects. [meseguer et al 1999, aguilar et al 1998])and the lowest density of glutathione peroxidase positive glial cells is found in the substantia nigra--leaving this dopaminergic cell group with less protection from oxidative stress and vulnerable to PD (Damier et al 1996) (there is a doc in Fla, Pearlman, who will give IV glutathione to PD patients and there is currently a study at the univ of fla (or one of the med schools in fla) looking at the use of IV glutathione in PD--please understand i am not endorsing the use of IV glutathione for PD-from my understanding, it should result in initial symptom improvements, but very soon loses effectiveness; i hope i am incorrect)

and of course statins interrupt the pathway to coenzyme q10 production.
I could continue, but the time is late and I have probably already typed more than anyone wants to read.
when I first joined the original BT group, I asked the question if anyone else suspected that statins were associated with their parkinson's disease. I was so bullied and ridiculed by one individual, who was joined by a few others who made fun of me and my "theories" (ie --we've been around long enough to hear all the theories and are immune to them, etc. etc. ) that I ceased from sharing my research findings with the group. I am not claiming to be correct--but questioning. so thank you, carolyn, for providing me an opening...it's Carolyn's fault, everyone........
in all seriousness, madelyn

[reverett123]

I, for one, am glad to hear your theories. Anyone who thinks they have "heard them all" is fooling themselves. Let's make a deal - I won't shut up if you won't.
-Rick

[Stitcher]

Olsen, I am taking Lipitor, and I have been on cholesterol med for many years. I am taking this information to my Internist.

It is interesting how far back the speculation goes, while it is only now that study has begun

Rick and Olsen, isn't that what boards like these are for...seeking help and information...sharing and debating views...etc.

smiley-linie-008.gif

SCIENCE NEWS (Reuters)
January 15, 2007
Renewed evidence suggests statin/Parkinson's link
http://www.sciam.com/article.cfm?cha...898497EB682C27


BMJ.com
Rapid Responses published:
http://www.bmj.com/cgi/eletters/325/7369/851

• Might statins cause Parkinsons? (18 October 2002)
• Coenzyme Q-10 Repletion (20 October 2002)
• Coenzyme Q vs levodopa for Parkinson's (21 October 2002)
• Re: Might statins cause Parkinsons? (24 October 2002)

Lipitor (atorvastatin and Related) - Rxboard
statin induced parkinson's-german med journal
Der Nevenarzt (German Medical Journal)
Date: Thursday, 30 December 2004, at 12:10 p.m.
http://www.rxlist.com/rxboard/lipito...ames;read=4267


Low LDL Levels Linked to Parkinson's Risk
By Neil Osterweil, Senior Associate Editor, MedPage Today
Reviewed by Zalman S. Agus, MD; Emeritus Professor at the University of Pennsylvania School of Medicine.
December 20, 2006
http://www.medpagetoday.com/Neurolog...isease/tb/4742

[olsen]

I am not suggesting anyone stop a medication without first discussing it with their doc--or even suggesting anyone stop a medication--but if you decide to do so, please know that most phisicians are not aware of the following (this info does not get big press--freq. published and forgotten)several studies conclude that individuals who stop statins cold turkey have a higher incidence of coronary events. many researchers theorized that obviously the statin was necessary to protect one from this cardiac event. It is true that statins are very powerful anti - inflammatories and also are wonderful at increasing perfusion everywhere--including those coronary arteries that may be blocked (for this reason I think they will be used in the future for SHORT term ACUTE settings--NOT as a life time drug)there is one study showing preliminary evidence that stopping a statin resulted in "rebound" increase in platelet stickiness, which peaked about day 14 in the study. Platelet adhesion is what contributes to clot formation within the arteries--so if platelet stickiness increases, the potential for clotting increases--and if one has plaques formed in coronary arteries, an increase in platelet stickiness may result in blockage of an artery. Does that mean one must STAY on a statin forever? Dr. Duane Graveline (whom Carolyn mentioned in her post) has guidelines to assist anyone going off a statin--he suggests first tapering off them (to decrease the "shock" of taking away a powerful anti-inflammatory and positive perfusion agent) and to also consider taking low dose aspirin (or plavix serves the same purpose if you are taking it) to decrease the platelet stickiness for whatever period of time your doc determinees to cover this "rebound platelet stickiness" period. His web site: www.spacedoc.net (the spacedoc does not refer to his cognitive abilities--he is an MD who was also an astronaut)
the primary reference:
Thromb Haemost. 2003 Sep;90(3):476-82. Related Articles, Links


Platelet hyperactivity after statin treatment discontinuation.


Puccetti L, Pasqui AL, Pastorelli M, Bova G, Di Renzo M, Leo A,
Cercignani M, Palazzuoli A, Auteri A, Bruni F.




Hydroxymethyl-glutaryl-CoA-reductase inhibitors (statins) reduce
cardiovascular events by cholesterol lowering as well as by
non-lipid related actions. Among them, the modulation of platelet
activity could play a relevant role in vascular protection.
Furthermore withdrawal of statins has been associated with
increased cardiovascular event rate. The aim of our study was to
evaluate platelet activity after cerivastatin discontinuation in
eighteen subjects that did not accept other drugs and in sixteen
subjects continuing treatment with simvastatin. Fourteen subjects
at the end of the discontinuation period decided to receive other
drugs (simvastatin) and they were evaluted six weeks later. We
measured complete lipid profile by the chromogenic method (LDL-C
was calculated); oxidized-LDL (ox-LDL; ELISA), platelet P-selectin
(P-sel) expression (flow cytometry detection), platelet
aggregation (% change of transmitted light), intracellular
citrullin production (iCit; HPLC) as an indicator of intracellular
NO synthase activity at baseline and 7, 14, 28, 60 days after
statin discontinuation. P-sel expression and platelet aggregation
were increased at 14 days (p < 0.001 and p < 0.05) in association
with raised ox-LDL (r = 0.30, p < 0.05) and decreased iCit (r =
0.53, p < 0.01). Increased LDL-C was related to P-sel and platelet
aggregation at 28 days (r = 0.30, p < 0.05). Subjects continuing
statin treatment had no significant changes of P-sel at 28 (p =
0.221) and 60 days (p = 0.238). Subjects treated with simvastatin
after 60 days of diet showed a significant reduction of P-sel and
platelet aggregation after six weeks of treatment (p < 0.01). Our
data suggest a platelet hyperactivation state in the second week
after statin discontinuation which is partially related to raised
LDL-C. Such a finding could participate in the increased
cardiovascular event rate after statin discontinuation.


Circulation. 2002 Mar 26;105(12):1446-52. Related Articles, Links


Comment in:
Circulation. 2002 Mar 26;105(12):e9085-90.
Circulation. 2003 Jan 28;107(3):e27.
Circulation. 2004 Oct 19;110(16):2280-2.

[lindylanka]

Very interesting stuff. Prompted by a friend who is about to start taking statins, I had thought of approaching my GP about them, but I think I will hang fire for the time being. As interesting as the actual issue surrounding the statins themselves is the following:

"it is important to determine the relation between brain fatty acids and PD because the brain fatty acid content depends on nutritional intake, a readily manipulable environmental factor"

Not just because such an intake COULD be used in future research into the causes of and/or cures for PD, but because of all the areas of food production that there are, the production of fats is the one where there have been immense changes, that are largely invisible, as they are often the hidden content in packaged foods. That is with the notable exception of margarines, and more modern butter substitutes which can be found in nearly everyones fridge.....and largely marketed as being more healthy than butter itself. Interesting too in light of the way that eggs are currently being 'rehabilitated' too..........