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In reply to the discussion: Reversing disease by reading random postings on a message board. [View all]HysteryDiagnosis
(19,342 posts)NO SIDE EFFECTS, an increase in ejection fraction in CHF patients, Protection of renal tissue in Type II diabetes, etc etc. First, he is DUing NO HARM.
http://www.ncbi.nlm.nih.gov/pubmed/22120862
Statin intolerance: Now a solved problem.
Sikka P, Kapoor S, Bindra VK, Sharma M, Vishwakarma P, Saxena KK.
Source
Department of Pharmacology, LLRM Medical College, Muradnagar, Ghaziabad, India.
Abstract
Statins are the most effective and widely used drugs for treating dyslipidemia, a major risk factor for coronary heart disease. These are one of the safest hypolipidemic drugs but many patients are bound to discontinue statins due to their side effects. Hepatotoxicity, myotoxicity and peripheral neuropathy are important out of them. Discontinuation of statins leads to dylipidemia and its grave consequences. Hence, there should be enough strategies for statin intolerant patients, so that they can be saved from these consequences.
These side effects can be avoided by the awareness of certain factors viz. potential drug interactions and dose adjustment according to patho-physiology of the patient. Baseline investigations for liver function and muscle toxicity should be done before initiating statin therapy. Here, we are discussing various options for statin intolerant hyperlipidemic patients such as lower and intermittent dosing of statins, alternate hypolipidemic drugs, red yeast rice, supplementation with coenzyme Q10 and vitamin D. A number of hypolipidemic drugs are in trial phases and hold promise for statin intolerant patients.
ASK yourself what this says EXACTLY:
http://www.ncbi.nlm.nih.gov/pubmed/20367194
TAKE HOME MESSAGE:
CoQ(10) does not cause serious adverse effects in humans and new formulations have been developed that increase CoQ(10) absorption. Oral CoQ(10) is a viable antioxidant strategy in many diseases, providing a significant to mild symptomatic benefit. Idebenone and MitoQ are promising substitutive CoQ(10)-related drugs which are well tolerated and safe.
http://www.ncbi.nlm.nih.gov/pubmed/19932599
In the field of mitochondrial myopathies, primary CoQ(10) deficiencies have been identified, involving different genes of the CoQ(10) biosynthetic pathway; some of these conditions were found to be highly responsive to CoQ(10) administration. The initial observations of CoQ(10) effects in Parkinson's and Huntington's diseases have been extended to Friedreich's ataxia, where CoQ(10) and other quinones have been tested. CoQ(10) is presently being used in a large phase III trial in Parkinson's disease. CoQ(10) has been found to improve sperm count and motility on asthenozoospermia. Moreover, for the first time CoQ(10) was found to decrease the incidence of preeclampsia in pregnancy. The ability of CoQ(10) to mitigate headache symptoms in adults was also verified in pediatric and adolescent populations.
http://www.ncbi.nlm.nih.gov/pubmed/21878067
Abstract
We studied effect of coenzyme Q(10) on 24-hour blood pressure profile and function of vascular endothelium in patients with essential hypertension. Coenzyme Q(10) was used as a component of combination therapy comprising angiotensin converting enzyme inhibitor enalapril. Administration of coenzyme Q(10) in combination with traditional antihypertensive therapy promoted normalization of vascular endothelial function and more effective correction of 24-hour blood pressure profile. These findings allow to consider the use of coenzyme Q(10) as promising component of combination therapy of arterial hypertension.
http://www.ncbi.nlm.nih.gov/pubmed/22172526
Diabetes-induced increases in total renal collagen but not glomerulosclerosis were significantly decreased with CoQ10 therapy. Mitochondrial superoxide and ATP production via complex II in the renal cortex were increased in db/db mice, with ATP normalized by CoQ10. However, excess renal mitochondrial hydrogen peroxide production and increased mitochondrial membrane potential seen in db/db mice were attenuated with CoQ10. Renal superoxide dismutase activity was also lower in db/db mice compared with dbH mice. Our results suggest that a deficiency in mitochondrial oxidized CoQ10 (ubiquinone) may be a likely precipitating factor for diabetic nephropathy. Therefore CoQ10 supplementation may be renoprotective in type 2 diabetes, via preservation of mitochondrial function.