Statins can also interfere with hormones such as testosterone, estrogen and vitamin D as these are made from cholesterol. In addition, by lowering cholesterol too much statins can interfere with cell to cell communication. Cells have dense regions of the plasma membrane known as lipid rafts which are enriched in cholesterol and sphingomyelin. Many receptors important in signal transduction tend to aggregate in these lipid rafts. Lowering cholesterol can disrupt the lipid rafts and interfere with these signal transduction receptors. Lastly, statins inhibit the production CoQ10 which is a critical molecule for the heart and other muscles.
Here is Dr. Sinatra's website which discusses the book.
In addition, both Dr. Sinatra and Dr. Bowden were interviewed in a recent episode of the People's Pharmacy. The podcast (mp3 recording) of this interview will be freely available for the next 3 weeks at http://www.peoplespharmacy.com/2013/03/ ... erol-myth/
Again, please read this book before using a statin as they could cause symptoms which may be indistinguishable from MS.
Video #1 http://www.doctoroz.com/episode/doctors ... erol-wrong
Video #2 inflammation, NOT chol, causes heart disease; statins = BAD
http://www.doctoroz.com/episode/doctors ... ideo=16021
Video #3 "Particle Size Test for LDL"
http://www.doctoroz.com/episode/doctors ... ideo=16022
Cholesterol article: http://www.doctoroz.com/videos/cholesterol-fact-sheet
Anti-inflammatory recipes: http://www.doctoroz.com/videos/anti-inf ... your-heart
Cholesterol Facts vs Myths: http://www.doctoroz.com/videos/choleste ... age=2#copy
Did Lipitor (Atorvastatin) Trigger Lou Gehrig's Disease?
http://www.peoplespharmacy.com/2013/03/ ... s-disease/
Did Cholesterol Drug Cause Man Boobs?
http://www.peoplespharmacy.com/2013/01/ ... man-boobs/
Kidney injury or failure with high dose statins.
http://www.peoplespharmacy.com/2013/03/ ... de-effect/
Canadian researchers tracked over 2 million patients from seven Canadian provinces as well as subjects in the U.S. and England. These were people put on statins between 1997 and 2008. Over 600,000 were receiving what are classed as high dose or high-potency statins.
The Canadian investigators discovered that when people were exposed to these "high-dose" or "high-potency" statins compared to either no statin, niacin, lower doses or lower-potency statins, they experienced an increased risk for kidney injury or failure. The damage was detectable within the first 4 months of treatment and remained elevated for at least two years. To be specific, those on high potency statins (as defined above) were 34% more likely to be hospitalized with acute kidney injury compared to the control patients.
High Dose or High-Potency Statins Defined:
Atorvastatin (Lipitor): 20 mg or more
Simvastatin (Zocor): 40mg or more
Rosuvastatin (Crestor): 10 mg or more
http://www.fda.gov/ForConsumers/Consume ... 293330.htm
FDA wrote:FDA has been investigating reports of cognitive impairment from statin use for several years. The agency has reviewed databases that record reports of bad reactions to drugs and statin clinical trials that included assessments of cognitive function.
The reports about memory loss, forgetfulness and confusion span all statin products and all age groups. Egan says these experiences are rare but that those affected often report feeling “fuzzy” or unfocused in their thinking.
In general, the symptoms were not serious and were reversible within a few weeks after the patient stopped using the statin. Some people affected in this way had been taking the medicine for a day; others had been taking it for years.
What should patients do if they fear that statin use could be clouding their thinking? “Talk to your health care professional,” Egan says. “Don’t stop taking the medication; the consequences to your heart could be far greater.”
http://www.peoplespharmacy.com/2013/05/ ... ld-you-so/
Decreased muscle mitochondria due to statins.
Increased risk of diabetes due to statin usage.Simvastatin attenuates increases in cardiorespiratory fitness and skeletal muscle mitochondrial content when combined with exercise training in overweight or obese patients at risk of the metabolic syndrome.
http://www.bmj.com/highwire/filestream/ ... /bmj.f2610
...there was an increased risk of incident diabetes with atorvastatin (adjusted hazard ratio 1.22, 95% confidence interval 1.15 to 1.29), rosuvastatin (1.18, 1.10 to 1.26), and simvastatin (1.10, 1.04 to 1.17).
http://www.nytimes.com/2013/11/14/opini ... atins.html
http://ccsviinms.blogspot.com/2013/08/m ... blood.html
Serum inflammation numbers (like c reactive protein) are a much better indicator of cardiovascular or endothelial risk, than LDL.
And there are lifestyle and nutrition modifications that can make a bigger difference in raising HDL, and help the brain.
http://ccsviinms.blogspot.com/2013/11/g ... brain.html
hope people really read the research you've compiled, before taking another pill--
dx dual jugular vein stenosis (CCSVI) 4/09
do not forget, it is not being used by MS patients for ANY cardiovascular effects.cheerleader wrote:Serum inflammation numbers (like c reactive protein) are a much better indicator ocardiovascular or endothelial risk, than LDL.
The spectrum of statin myopathy
http://journals.lww.com/co-rheumatology ... hy.13.aspx
Purpose of review: This review discusses the spectrum of myopathies associated with statin use, with special attention given to a recently identified statin-associated autoimmune-necrotizing myopathy. The clinical characteristics of these patients, pathologic findings, associated autoantibody and immunogenetic risk factors are discussed.
Recent findings: In the past several years, a novel form of autoimmunemyopathy associated with statin use has been described. Patients with this form of myositis have unique clinical, pathologic and pathophysiologic features when compared with those with self-limited statin toxic myopathy. An autoantibody directed against HMG-CoA reductase (HMGCR), the pharmacologic target of statins, characterizes the disease and can be used in clinical practice to identify these patients and direct therapy. Still, many questions remain to be answered regarding the pathogenic mechanisms at play, risk factors for developing the disease, long-term prognosis and effects of rechallenge with statins or other cholesterol-lowering drugs.
Summary: Statins can cause a spectrum of muscle diseases, most of which are self-limited and improve with discontinuation of the offending agent. In a subgroup, an autoimmune necrotizing myopathy develops that persists after discontinuation of statins. Specific autoantibody testing can help identify these patients in clinical practice and determine the need for immunosuppressive therapy.
Am J Pathol. 2009 May;174(5):1880-90.
- Remyelination of lesions in the central nervous system contributes to neural repair following clinical relapses in multiple sclerosis. Remyelination is initiated by recruitment and differentiation of oligodendrocyte progenitor cells (OPCs) into myelinating oligodendrocytes. Simvastatin, a blood-brain barrier-permeable statin in multiple sclerosis clinical trials, has been shown to impact the in vitro processes that have been implicated in remyelination. Animals were fed a cuprizone-supplemented diet for 6 weeks to induce localized demyelination in the corpus callosum; subsequent return to normal diet for 3 weeks stimulated remyelination. Simvastatin was injected intraperitoneally during the period of coincident demyelination and OPC maturation (weeks 4 to 6), throughout the entire period of OPC responses (weeks 4 to 9), or during the remyelination-only phase (weeks 7 to 9). Simvastatin treatment (weeks 4 to 6) caused a decrease in myelin load and both Olig2(strong) and Nkx2.2(strong) OPC numbers. Simvastatin treatment (weeks 4 to 9 and 7 to 9) caused a decrease in myelin load, which was correlated with a reduction in Nkx2.2(strong) OPCs and an increase in Olig2(strong) cells, suggesting that OPCs were maintained in an immature state (Olig2(strong)/Nkx2.2(weak)). NogoA+ oligodendrocyte numbers were decreased during all simvastatin treatment regimens. Our findings suggest that simvastatin inhibits central nervous system remyelination by blocking progenitor differentiation, indicating the need to monitor effects of systemic immunotherapies that can access the central nervous system on brain tissue-repair processes.
Pharmazie. 2014 Jun;69(6):448-54.
- Statins are commonly prescribed lipid-lowering medications that significantly reduce the risk of cardiovascular events. In addition to their ability to lower cholesterol by affecting the rate-limiting step in cholesterol biosynthesis, statins also have anti-inflammatory, immunomodulatory, antioxidant, antiapoptotic, and antiplatelet effects. Because of these pleiotropic abilities, statins may have some beneficial effects on neurologic diseases, including cerebrovascular disease, neurodegenerative disease, multiple sclerosis, and brain tumors. Although statins are a well-tolerated class of drugs, they also have potential adverse effects (AEs). A growing body of evidence indicates that statins may have potential negative effects on nervous system-associated diseases, including myopathies, peripheral neuropathy, intracerebral hemorrhage (ICH), and other diseases of the central nervous system (e.g., cognitive impairment, depression, sleep disorders, nightmare, and headache). Clinicians, especially neurologists, should be aware of the potential risk of neuropathy in patients who take statins.
http://www.peoplespharmacy.com/2014/10/ ... too-low-2/
Dr. David L. Tirschwell reported to the American Heart Association in 1999 that people with cholesterol under 180 had twice the risk of strokes caused by bleeding into the brain as those with cholesterol counts around 230.
Cholesterol may also affect neurochemistry. Researchers have been puzzled by the recurrent association of low cholesterol and violent death, especially from suicide. Cholesterol that is very low may alter mood and affect behavior in ways that are not completely understood.
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