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Old 03-21-2010, 07:44 AM
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mrsD mrsD is offline
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mrsD mrsD is offline
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Join Date: Aug 2006
Location: Great Lakes
Posts: 33,508
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Welcome to NeuroTalk.

This subject of statins is becoming HUGE.

I gave a link to a post in the Metanx thread where I give some of the newest info, here it is again:

http://neurotalk.psychcentral.com/sh...ghlight=statin

Post #3 there gives the link to a PDF which is pretty new, listing all the problems of statins based on previous studies. There is more on post #6.

Also Medication Sense by Dr. Cohen MD...his link is good too.
He has book you get on the subject.

Also Dr. Graveline MD has a site and book on Lipitor and what is did to HIM.

All those links are on that thread.

Here is another.
http://www.thincs.org/links.htm
http://www.ravnskov.nu/cholesterol.htm

Just type in "cholesterol myth" into Google. You can spend days reading from that one search.

Dr. Cohen has a study on his website that reveals how doctors dismiss side effects, from statins, because they don't understand them, or have been lied to by drug reps.
http://www.medicationsense.com/artic...cts012108.html

People who have a stent like you do, are in a very difficult place.
Finding information on stent recipients not using a drug compared to those who do use one, will be hard to find. Many studies are done by the drug companies themselves.
PubMed link is above, and you can click that, and search "stent statin" and 239 papers will come up.
This one shows no difference between Lipitor use combined with Plavix, vs no Lipitor. (and it is from another country Korea)
http://www.ncbi.nlm.nih.gov/pubmed/19372620
Quote:
Circ J. 2009 Jun;73(6):1111-8. Epub 2009 Apr 17.
Comparison of low vs moderate dose of atorvastatin in clopidogrel resistance after coronary stenting in Korean patients with acute coronary syndrome.

Hong SJ, Park JY, Kim KA, Ahn CM, Park JS, Kim YH, Shim WJ, Park SM, Lim DS.

Department of Cardiology, Cardiovascular Center, Korea University Anam Hospital, Seoul, Korea.

BACKGROUND: The effect of atorvastatin 10 mg vs 40 mg in clopidogrel resistance and clinical events after coronary stenting was compared in patients with acute coronary syndrome (ACS). METHODS AND RESULTS: Platelet aggregation was measured before clopidogrel administration and 4 h, 24 h, 5 days, and 8 months later in 130 ACS patients. Stented patients were randomly assigned to atorvastatin either 10 mg (n=65) or 40 mg (n=65), and received an oral loading dose of 300 mg of clopidogrel followed by 75 mg/day for 8 months. Measurement of platelet aggregation was done by the turbimetric method. The mean % changes in inhibition of platelet aggregation were 35.5 +/-8.3, 50.9 +/-10.1, 38.3 +/-8.3, 40.0 +/-6.8 in the Atorvastatin 10 mg Group and 31.0 +/-7.6, 43.7 +/-9.8, 45.0 +/-10.3, 43.5 +/-7.8 (4 h, 24 h, 5 days, and 8 months, respectively, after 300 mg of clopidogrel pretreatment) in the Atorvastatin 40 mg Group with no significant differences between the 2 groups. Cardiovascular events showed no significant differences during the follow-up. CONCLUSIONS: Atorvastatin 10 mg or 40 mg co-administered with clopidogrel for 8 months did not affect the antiplatelet potency of clopidogrel and showed no significant differences in the clinical events in ACS patients.

PMID: 19372620 [PubMed - indexed for MEDLINE]
On the other hand there are papers there favorable to statins following stenting (many from USA funded with Big Pharm money).

This new video from Univ Cal SF... is long but it describes which LDL fractions are very harmful... the very low LDL which are not tested routinely. Evidently the new thought is that regular LDL are not dangerous, but the VL LDL is. That "thought" may change as well, like everything else in medicine!
http://www.youtube.com/watch?v=dBnniua6-oM
You can improve your future by just avoiding sugar and fructose!
The video is long, but worth it in the end. The cholesterol portion is about in the middle.

Realize that the massive mountain of information on statins has be compiled by the drug companies to convince doctors to use them. They are very persuasive. But many doctors over time, have come to realize that there is more to the story.
The amount of homework you will have to do in order to decide if you are to change your therapy, is very large. It is a personal decision, and will have to be discussed with your doctor. Expect a battle... I have one with my own doctor frequently.

Endothelial inflammation is the start of plaque. You can reduce that risk with quality curcumin product (which reduced endothelial inflammation as much as a statin...Lipitor.
Quote:
Drugs R D. 2008;9(4):243-50.
Effect of NCB-02, atorvastatin and placebo on endothelial function, oxidative stress and inflammatory markers in patients with type 2 diabetes mellitus: a randomized, parallel-group, placebo-controlled, 8-week study.

Usharani P, Mateen AA, Naidu MU, Raju YS, Chandra N.

Department of Clinical Pharmacology and Therapeutics, Nizam's Institute of Medical Sciences, Hyderabad, Andhra Pradesh, India.

BACKGROUND AND OBJECTIVE: Hyperglycaemia leads to increased oxidative stress resulting in endothelial dysfunction. ACE inhibitors, antioxidants and HMG-CoA reductase inhibitors (statins) have been shown to improve endothelial function. The aim of this study was to compare the effects of NCB-02 (a standardized preparation of curcuminoids), atorvastatin and placebo on endothelial function and its biomarkers in patients with type 2 diabetes mellitus. METHODS: A total of 72 patients with type 2 diabetes were randomized to receive NCB-02 (two capsules containing curcumin 150 mg twice daily), atorvastatin 10 mg once daily or placebo for 8 weeks. Endothelial function assessment was performed at baseline and post-treatment using digital volume plethysmography (salbutamol [albuterol] challenge test) to measure change in reflective index, an indicator of arterial vascular tone. Blood samples were similarly collected at baseline and post-treatment for estimations of malondialdehyde, endothelin-1 (ET-1), interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNFalpha). Pre-and post-treatment safety assessments were also conducted. ANOVA and paired t-test evaluations were used for comparison. RESULTS: A total of 67 patients completed the study. At baseline, there was no significant difference in the various parameters tested. In all three groups, the change in reflective index at baseline was <6% as assessed by the salbutamol challenge test, indicating the presence of endothelial dysfunction. Compared with baseline, there was a significant improvement in endothelial function after treatment with atorvastatin (mean +/- SD: -3.63 +/- 3.17% vs -8.95 +/- 6.80%, respectively) and NCB-02 (-2.69 +/- 3.02% vs -8.19 +/- 5.73%, respectively). Similarly, patients receiving atorvastatin or NCB-02 showed significant reductions in the levels of malondialdehyde, ET-1, IL-6 and TNFalpha. No significant improvements were obtained in patients administered placebo. CONCLUSION: NCB-02 had a favourable effect, comparable to that of atorvastatin, on endothelial dysfunction in association with reductions in inflammatory cytokines and markers of oxidative stress. Further studies are needed to evaluate the potential long-term effects of NCB-02 and its combination with other herbal antioxidants.

PMID: 18588355 [PubMed - indexed for MEDLINE]
You can reduce C-reactive protein with Vit C.
Quote:
Free Radic Biol Med. 2009 Jan 1;46(1):70-7. Epub 2008 Oct 10.
Vitamin C treatment reduces elevated C-reactive protein.

Block G, Jensen CD, Dalvi TB, Norkus EP, Hudes M, Crawford PB, Holland N, Fung EB, Schumacher L, Harmatz P.

University of California, Berkeley, 94720, USA. gblock@berkeley.edu

Plasma C-reactive protein (CRP) is an inflammatory biomarker that predicts cardiovascular disease. Lowering elevated CRP with statins has reduced the incidence of cardiovascular disease. We investigated whether vitamin C or E could reduce CRP. Healthy nonsmokers (N=396) were randomized to three groups, 1000 mg/day vitamin C, 800 IU/day vitamin E, or placebo, for 2 months. Median baseline CRP was low, 0.85 mg/L. No treatment effect was seen when all participants were included. However, a significant interaction was found, indicating that treatment effect depends on baseline CRP concentration. Among participants with CRP indicative of elevated cardiovascular risk (> or =1.0 mg/L), vitamin C reduced the median CRP by 25.3% vs placebo (p=0.02) (median reduction in the vitamin C group, 0.25 mg/L, 16.7%). These effects are similar to those of statins. The vitamin E effect was not significant. In summary, treatment with vitamin C but not vitamin E significantly reduced CRP among individuals with CRP > or =1.0 mg/L. Among the obese, 75% had CRP > or =1.0 mg/L. Research is needed to determine whether reducing this inflammatory biomarker with vitamin C could reduce diseases associated with obesity. But research on clinical benefits of antioxidants should limit participants to persons with elevations in the target biomarkers.

PMID: 18952164 [PubMed - indexed for MEDLINE]
These studies however, I would expect not to be given to doctors by the drug reps. So they probably don't even know they exist.

When you search on PubMed, if you decide to, use only generic names for drugs, and keyword carefully. To get the Vit C paper, I used "c-reactive protein statin" as a keyword.

The drug industry does its slanting with other drugs too, and this "statin" issue is just one of many these days.

It will be your decision after doing this homework as to your future. I cannot "tell" you what to do, but I do think patients need ALL the information concerning drugs, to make informed decisions.

And if you are not taking a quality CoQ-10 product, now would be the time to start.
__________________
All truths are easy to understand once they are discovered; the point is to discover them.-- Galileo Galilei

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