I just sent you a PM about statin risks, vit D and folate benefits:
, http://www.ivanhoe.com/channels/p_ch...?storyid=10491Blocks CoQ10 production.
CoQ10 is a coenzyme necessary for the production of ATP (adenosine triphosphate). ATP is the source for cellular energy within the human heart. As CoQ10 is diminished, the heart weakens. Over time, this can result in congestive heart failure (CHF).http://www.leaflady.org/statin_risks.htm
Liver damage, muscle pain: http://www.mayoclinic.com/health/sta...SECTIONGROUP=2
: http://www.medscape.com/viewarticle/496431_4peripheral neuropathy
, or pain or numbness in the extremities like fingers and toes: http://seniorjournal.com/NEWS/Health...rchersFind.htm
"Statin-associated peripheral neuropathy may persist for months or years after withdrawal of the statin. In two ADRAC cases of persistent peripheral neuropathy, motor and sensory conduction tests showed minimal recovery 4 and 12 months, respectively, after discontinuation of simvastatin, despite clinical improvement. A further 21 cases had not recovered at the time of reporting, between one and eight months after discontinuation of the statin. In two other reports, the problem was persisting after 3 and 5 years, respectively." http://www.procor.org/research/resea...?doc_id=982615cancer risk: http://www.cancerdecisions.com/conte.../lang,english/
Statins can also cause your CPK levels to be mildly elevated.Strokes:
The cholesterol-lowering medication atorvastatin (Lipitor) may slightly increase the risk of hemorrhagic stroke, or bleeding in the brain, when taken by people who have already had a stroke, according to a Duke University Medical Center researcher. But it also reduces the risk of having a second stroke or coronary heart event.http://www.dukehealth.org/HealthLibrary/News/10199
==============Cholesterol Is Not A Major Cause Of Arterial Disease
Several factors appear to be of greater importance than cholesterol in causing arterial disease. Among these are deposition of toxic metals in the lining endothelium of arteries, Vitamin C deficiency, excessive amounts of lipoprotein (a), inflammation in arteries, excessive clotting of blood, homocysteine elevation (hyperhomocystinemia) and dangerous foods.
An important study by Dr. Harlan Krumholz revealed that persons with low cholesterol levels over the age of 70 died twice as often from heart attacks as older persons with high cholesterol values. Most studies in old persons have shown that cholesterol is not a risk factor for coronary artery disease. Approximately 90 % of cardiovascular disease is seen in persons over 60 years of age. Almost all studies have shown that high cholesterol is not a risk factor for women. This leaves cholesterol as a risk factor for less than 5 % of those persons dying of a heart attack.
High cholesterol values protect against infection. In a review of 19 studies involving 68,000 persons low cholesterol values revealed an increased risk for dying from lung and gastrointestinal diseases. Both lung and g.i. diseases are often related to infections.http://www.newswithviews.com/Howenstine/james23.htm
====Benefits of High Cholesterol:http://www.westonaprice.org/moderndi...s_cholest.htmlhttp://medicalconsumers.org/2003/06/...erence-report/
1. Krumholz HM and others. Lack of association between cholesterol and coronary heart disease mortality and morbidity and all-cause mortality in persons older than 70 years. Journal of the American Medical Association 272, 1335-1340, 1990.
2. Ravnskov U. High cholesterol may protect against infections and atherosclerosis. Quarterly Journal of Medicine 96, 927-934, 2003.
3. Jacobs D and others. Report of the conference on low blood cholesterol: Mortality associations. Circulation 86, 1046–1060, 1992.
4. Iribarren C and others. Serum total cholesterol and risk of hospitalization, and death from respiratory disease. International Journal of Epidemiology 26, 1191–1202, 1997.
5. Iribarren C and others. Cohort study of serum total cholesterol and in-hospital incidence of infectious diseases. Epidemiology and Infection 121, 335–347, 1998.
6. Claxton AJ and others. Association between serum total cholesterol and HIV infection in a high-risk cohort of young men. Journal of acquired immune deficiency syndromes and human retrovirology 17, 51–57, 1998.
7. Neaton JD, Wentworth DN. Low serum cholesterol and risk of death from AIDS. AIDS 11, 929–930, 1997.
8. Rauchhaus M and others. Plasma cytokine parameters and mortality in patients with chronic heart failure. Circulation 102, 3060-3067, 2000.
9. Niebauer J and others. Endotoxin and immune activation in chronic heart failure. Lancet 353, 1838-1842, 1999.
10. Vredevoe DL and others. Skin test anergy in advanced heart failure secondary to either ischemic or idiopathic dilated cardiomyopathy. American Journal of Cardiology 82, 323-328, 1998.
11. Rauchhaus M, Coats AJ, Anker SD. The endotoxin-lipoprotein hypothesis. Lancet 356, 930–933, 2000.
12. Rauchhaus M and others. The relationship between cholesterol and survival in patients with chronic heart failure. Journal of the American College of Cardiology 42, 1933-1940, 2003.
13. Horwich TB and others. Low serum total cholesterol is associated with marked increase in mortality in advanced heart failure. Journal of Cardiac Failure 8, 216-224, 2002.
14. Elias ER and others. Clinical effects of cholesterol supplementation in six patients with the Smith-Lemli-Opitz syndrome (SLOS). American Journal of Medical Genetics 68, 305–310, 1997.
15. Bhakdi S and others. Binding and partial inactivation of Staphylococcus aureus a-toxin by human plasma low density lipoprotein. Journal of Biological Chemistry 258, 5899-5904, 1983.
16. Flegel WA and others. Inhibition of endotoxin-induced activation of human monocytes by human lipoproteins. Infection and Immunity 57, 2237-2245, 1989.
17. Weinstock CW and others. Low density lipoproteins inhibit endotoxin activation of monocytes. Arteriosclerosis and Thrombosis 12, 341-347, 1992.
18. Muldoon MF and others. Immune system differences in men with hypo- or hypercholesterolemia. Clinical Immunology and Immunopathology 84, 145-149, 1997.
19. Feingold KR and others. Role for circulating lipoproteins in protection from endotoxin toxicity. Infection and Immunity 63, 2041-2046, 1995.
20. Netea MG and others. Low-density lipoprotein receptor-deficient mice are protected against lethal endotoxemia and severe gram-negative infections. Journal of Clinical Investigation 97, 1366-1372, 1996.
21. Harris HW, Gosnell JE, Kumwenda ZL. The lipemia of sepsis: triglyceride-rich lipoproteins as agents of innate immunity. Journal of Endotoxin Research 6, 421-430, 2001.
22. Netea MG and others. Hyperlipoproteinemia enhances susceptibility to acute disseminated Candida albicans infection in low-density-lipoprotein-receptor-deficient mice. Infection and Immunity 65, 2663-2667, 1997.
23. Ross R, Glomset JA. The pathogenesis of atherosclerosis. New England Journal of Medicine 295, 369-377, 1976.
24. Ross R. The pathogenesis of atherosclerosis and update. New England Journal of Medicine 314, 488-500, 1986.
25. Klotz O, Manning MF. Fatty streaks in the intima of arteries. Journal of Pathology and Bacteriology. 16, 211-220, 1911.
26. At least 200 reviews about the role of infections in atherosclerosis and cardiovascular disease have been published; here are a few of them: a) Grayston JT, Kuo CC, Campbell LA, Benditt EP. Chlamydia pneumoniae strain TWAR and atherosclerosis. European Heart Journal Suppl K, 66-71, 1993. b) Melnick JL, Adam E, Debakey ME. Cytomegalovirus and atherosclerosis. European Heart Journal Suppl K, 30-38, 1993. c) Nicholson AC, Hajjar DP. Herpesviruses in atherosclerosis and thrombosis. Etiologic agents or ubiquitous bystanders? Arteriosclerosis Thrombosis and Vascular Biology 18, 339-348, 1998. d) Ismail A, Khosravi H, Olson H. The role of infection in atherosclerosis and coronary artery disease. A new therapeutic target. Heart Disease 1, 233-240, 1999. e) Kuvin JT, Kimmelstiel MD. Infectious causes of atherosclerosis. f.) Kalayoglu MV, Libby P, Byrne GI. Chlamydia pneumonia as an emerging risk factor in cardiovascular disease. Journal of the American Medical Association 288, 2724-2731, 2002.
27. Grau AJ and others. Recent bacterial and viral infection is a risk factor for cerebrovascular ischemia. Neurology 50, 196-203, 1998.
28. Mattila KJ. Viral and bacterial infections in patients with acute myocardial infarction. Journal of Internal Medicine 225, 293-296, 1989.
29. The successful trials: a) Gurfinkel E. Lancet 350, 404-407, 1997. b) Gupta S and others. Circulation 96, 404-407, 1997. c) Muhlestein JB and others. Circulation 102, 1755-1760, 2000. d) Stone AFM and others. Circulation 106, 1219-1223, 2002. e) Wiesli P and others. Circulation 105, 2646-2652, 2002. f) Sander D and others. Circulation 106, 2428-2433, 2002.
30. The unsuccessful trials: a) Anderson JL and others. Circulation 99, 1540-1547, 1999. b) Leowattana W and others. Journal of the Medical Association of Thailand 84 (Suppl 3), S669-S675, 2001. c) Cercek B and others. Lancet 361, 809-813, 2003. d) O’Connor CM and others. Journal of the American Medical Association. 290, 1459-1466, 2003.
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=============Vitamin D is Synthesized From Cholesterol and Found in Cholesterol-Rich Foods
One of cholesterol's many functions in the body is to act as a precursor to vitamin D.
Vitamin D can also be obtained from foods. Interestingly, foods that provide this vitamin -- all of which are animal foods -- tend to be high in cholesterol.
Since cholesterol is a precursor to vitamin D, inhibiting the synthesis of cholesterol will also inhibit the synthesis of vitamin D. Since sunlight is required to turn cholesterol into vitamin D, avoiding the sun will likewise undermine our ability to synthesize vitamin D. And since vitamin D-rich foods are also rich in cholesterol, low-cholesterol diets are inherently deficient in vitamin D. http://www.cholesterol-and-health.com/Vitamin-D.html
======The Right Fats
The assimilation and utilization of vitamin D is influenced by the kinds of fats we consume. Increasing levels of both polyunsaturated and monounsaturated fatty acids in the diet decrease the binding of vitamin D to D-binding proteins. Saturated fats, the kind found in butter, tallow and coconut oil, do not have this effect. Nor do the omega-3 fats.66 D-binding proteins are key to local and peripheral actions of vitamin D. This is an important consideration as Americans have dramatically increased their intake of polyunsaturated oils (from commercial vegetable oils) and monounsaturated oils (from olive oil and canola oil) and decreased their intake of saturated fats over the past 100 years.
In traditional diets, saturated fats supplied varying amounts of vitamin D. Thus, both reduction of saturated fats and increase of polyunsaturated and monounsaturated fats contribute to the current widespread D deficiency.Trans fatty acids
, found in margarine and shortenings used in most commercial baked goods, should always be avoided. There is evidence that these fats can interfere with the enzyme systems the body uses to convert vitamin D in the liver.80http://www.westonaprice.org/basicnut...ndmiracle.html
Debunking the Cholesterol Myth: http://www.drcranton.com/Cholesterol_myth.htm
We’re lead to believe that cholesterol is an enemy, particularly to cardiovascular health. But think about it, why does your liver naturally produce something that’s detriment to your health? It doesn’t.
Through tapes on the raft, the lipid hypothesis reigns supreme. It dictates that in order to stay healthy you should reduce your cholesterol (to an ever receding value) by consuming a low fat diet and exercise (no prob with latter though!). And If that fails you should try controversial medicines called statins.
They are notable for alarming side effects.
Sounds nice and simple? In England 2003, the average cholesterol value was 6.1, in France it was 6.2. The recommended cholesterol level is < 5mmol. This means a lot of people ’suffer’ from a symptomless disease. But here’s the best bit: our local French neighbours don’t suffer from heart disease much, definitely not as much as us. In Japan (2005), the level of cholesterol went up as their rate of heart disease dropped, perhaps because their general lifestyle is better than the Brits to avoid inflammation of the heart in the first place despite possible low vit D. Populations with the least level of cholesterol saw higher rates of heart disease. But furthermore, high cholesterol for women the world over is not a risk factor. Are they really that different?
Did you know that vitamin D is created from cholesterol? Provide your skin with adequate sunlight and excess cholesterol is turned into vitamin D, a hormone with responsibilities including calcium metabolisation, blood sugar regulation, blood pressure regulation, mental health function, diabetes prevention…
And if your excess cholesterol isn’t turned into D, it accumulates doesn’t it?…I can find no answers, at least online that refutes or proves this. Therefore could high cholesterol just be a signifier of low vitamin D, a hormone that is said to have anti-inflammatory properties?…http://moblogs.wordpress.com/2007/08...-significance/
When the men were grouped according to vitamin D intake above and below 2.5 mug and serum cholesterol levels above or below 250 mg %, a significant relationship appeared (using Yates's correction X2=10.3, P=0.0013 and the correlation coefficient 0.011 less than P less than 0.005). http://www.ncbi.nlm.nih.gov/pubmed/1179189Effects of Atorvastatin on vitamin D levels in patients with acute ischemic heart disease.:
In conclusion, atorvastatin increases vitamin D levels. This increase could explain some of the beneficial effects of atorvastatin at the cardiovascular level that are unrelated to cholesterol levels. http://www.ncbi.nlm.nih.gov/pubmed/17398180It ain't lowering cholesterol (which the liver regulates anyway) which lowers heart risk, from my reading. There are many reasons why the dietary-heart-cholesterol hypothesis should be questioned, and why statins might be acting in some other way to reduce the risk of coronary heart disease. Here, I propose that rather than being cholesterol-lowering drugs per se, statins act as vitamin D analogues, and explain why.
This proposition is based on published observations that the unexpected and unexplained clinical benefits produced by statins have also been shown to be properties of vitamin D. It seems likely that statins activate vitamin D receptors. http://www.ncbi.nlm.nih.gov/pubmed/16815382
=======Cholesterol: Friend Or Foe?http://www.westonaprice.org/knowyour...ol-friend.html
How Do High-Folate Diets Protect Against Heart Disease? http://www.medicalnewstoday.com/articles/40413.phphttp://howtopreventheartdisease.blog...by-folate.htmlhttp://ods.od.nih.gov/factsheets/folate.aspFolate Consumption Reduces Risk of Stroke by 20 Percent in Male Smokers http://www.naturalnews.com/025324_st...late_food.htmlFolate, brain health and stroke
and allergies: http://www.naturalnews.com/026225_fo...allergies.html