Results of the JUPITER study seemed to show that the statin drug Crestor lowers the risk of heart attacks and strokes in those with high levels of inflammation. Some believe this will lead to even more people being put on statin drugs.
In reality the benefits are actually insignificant. Aproximately 0.72 percent of the statin takers in the trial had a heart attack or stroke, compared with 1.5 percent of those taking placebos.
Instead of taking statin drugs that come with dangerous side effects, there are things you can do to reduce inflammation naturally.
Stop smoking. Smoking increases inflammation and your risk of cardiovascular disease. But research shows you can reverse all the damaging effects to your arteries within 10 years of quitting.
Olive oil and fish. Consuming olive oil and omega-3 fatty acids fight inflammation.
Get of the couch. Exercise a great way to lower stress and inflammation without any of the side effects associated with medications.
Get your sleep. Some research shows that both too little and too much sleep increases inflammation. The American Academy of Sleep Medicine says most adults need between seven and eight hours of sleep each night.
Reduce stress. High levels of stress hormones can lead to the release of excess inflammatory chemicals.
In order to believe the fallacy of statin efficacy one must first believe in the biggest and most dangerous scam in American history, the lipid hypothesis. The scientific data past or present does not support the assertion cholesterol (LDL) causes CVD.
The results from five large studies including more than 30,000 individuals have been published. Total cholesterol was lowered an average of 20.4%. The degree of cholesterol lowering had no association with lower incidence of CVD. If lowering cholesterol levels are so important in combating CVD why didn?t people whose cholesterol levels decreased the most get more of a benefit from the drugs? This is a real case for lack of exposure response which indicates that the factor under investigation is not the true cause, but is secondary to the real cause. (Ravnskov, Uffe. The Cholesterol Myths: Exposing the Fallacy that Saturated fat and Cholesterol cause heart disease.)
An analysis of all the big statin studies reported before 2000 found that long term use of the cholesterol lowering drugs for prevention of CVD produced a 1% greater risk of death over ten years compared to placebo groups. These findings are more than enough to negate the use of statins for the purpose of lowering the mortality rate in patients with a CVD risk. (British J of Clinical Pharmacology. 2001;52(4): 439-446)
?The JUPITER study stopped because of irrefutable benefit!?? Look at the numbers not just the percentages. The rates of the primary endpoint were .52 per 100 individuals. That’s .52%, compared to a 50% drop in cholesterol levels. As I said, the benefits are insignificant and do not even correlate to lowered cholesterol numbers. Medscape.com, please.
Lavaza? This is a shit product GalaxoSmithKline through out there to jump on the O-3 band wagon. It?s a fairly low dose product, and is extremely expensive. 1 cap equals 840mg of O-3. ?The benefits from O-3s is only attained from absurd amounts?? That?s absurd.
This is going to be like arguing with a 10-year-old. Anyone who actually has questions regarding statins or cholesterol should talk to their doctor or pharmacist.
This is a nice summary of the information Mr. Furci is neglecting, (and will try to discount) for anyone interested.
Coronary heart disease (CHD) is a major cause of morbidity and mortality worldwide. Elevated low density lipoprotein-cholesterol (LDL-C) and reduced high density lipoprotein-cholesterol (HDL-C) levels are well recognised CHD risk factors, with recent evidence supporting the benefits of intensive LDL-C reduction on CHD risk. Such observations suggest that the most recent National Cholesterol Education Program Adult Treatment Panel III guidelines, with LDL-C targets of 2.6 mmol/L, may result in under-treatment of a significant number of patients and form the basis for the proposed new joint European Societies treatment targets of 2 and 4 mmol/L, respectively, for LDL and total cholesterol. HMG-CoA reductase inhibitors (statins) reduce LDL-C by inhibiting the rate-limiting step in cholesterol biosynthesis and reduced CHD event rates in primary and secondary prevention trials. The magnitude of this effect is not fully accounted for by LDL-C reduction alone and may relate to effects on other lipid parameters such as HDL-C and apolipoproteins B and A-I, as well as additional anti-inflammatory effects. With increasing focus on the benefits of intensive cholesterol reduction new, more efficacious statins are being developed. Rosuvastatin is a potent, hydrophilic enantiomeric statin producing reductions in LDL-C of up to 55%, with about 80% of patients reaching European LDL-C treatment targets at the 10 mg/day dosage. The Heart Protection Study (HPS) demonstrated that LDL-C reduction to levels as low as 1.7 mmol/L was associated with significant clinical benefit in a wide range of high-risk individuals, including patients with type 2 diabetes mellitus, or peripheral and cerebrovascular disease, irrespective of baseline cholesterol levels, with no apparent lower threshold for LDL-C with respect to risk. Various large endpoint trials, including Treating to New Targets (TNT) and Study of Effectiveness of Additional reductions in Cholesterol and Homocysteine (SEARCH) will attempt to further address the issue of optimal LDL-C reduction. At low LDL-C levels, HDL-C becomes an increasingly important risk factor and is the primary lipid abnormality in over half of CHD patients, with the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study set to assess the effect of raising HDL-C on cardiovascular events in patients with low HDL-C and LDL-C levels below 3 mmol/L. A variety of agents are being developed, which affect both LDL-C and HDL-C metabolism, including inhibitors of acyl-coenzyme A-cholesterol acyl transferase, microsomal transfer protein and cholesterol ester transfer protein, as well as specific receptor agonists. Ezetimibe is a selective cholesterol absorption inhibitor, which produces reductions in LDL-C of up to 25 and 60% reduction in chylomicron cholesterol content with a 10 mg/day dosage. A 1 mmol/L reduction in LDL-C results in a 25% reduction in cardiovascular risk, independent of baseline LDL-C levels. Growing evidence supports the concept that lower is better for LDL-C and that increasing HDL-C represents an important therapeutic target. Furthermore, there is growing appreciation of the role of inflammation in atherogenesis. Consequently, increasing numbers of people should receive lipid-regulating therapy with the development of newer agents offering potential mechanisms of optimising lipid profiles and thus risk reduction. In addition, the pleiotropic anti-inflammatory effects of lipid lowering therapy may provide further risk reduction.
Drugs. 2004;64(11):1181-96.
What you and so many in the medical field fail to realize is that for a scientific hypothesis to be sound, it must agree with all observations. A hypothesis is not like a sports event, where the team with the greatest points wins. Even one observation that does not support a hypothesis is enough to disprove it. The lipid hypothesis is a bust. Cholesterol levels have never been shown to correlate with CVD. If cholesterol levels were so important, why doesn?t it matter whether we lower it by large or small amounts?
There are several hundred risk factors for CVD and cholesterol levels or ratios haven?t been shown to have any significance. In fact, approximately one fifth of the hearts of people who have died from heart attack have been shown in studies to have no coronary atherosclerosis. Almost half of all heart attack victims have what is considered normal cholesterol levels.
Continuing the outrageous claim that satins are potentially life saving because they lower cholesterol, is a huge scientific deception. Open your eyes. What you posted above shows nothing. Again, look at the actual numbers. Reduced mortality, which many studies don?t show, has no relationship to the amount of reduction in cholesterol levels. This, as stated in an earlier post, is a lack of exposure response. It proves the factor under investigation, cholesterol, is not the real cause.
Why don?t you turn your attention to oxidized VLDL and triglycerides, which are raised by eating sugars, especially fructose? To say that LDL is the ?bad? cholesterol and HDL is the ?good? cholesterol is hilarious. Again, show me the numbers. More-over, how about polyunsaturated fats role in CVD, which comprise 75% of the fat in plaque. Why is the incidence of CVD so much higher in people with hypertension independent of cholesterol levels? Why is it that arteries that pass through bony channels like the skull and few branches that pass through the heart muscle never become sclerotic independent of cholesterol levels? Why is it that veins never become sclerotic? Don?t worry I know the answers. Do you? If you did you wouldn?t be making such ridiculous posts.
Open your eyes AB. The pharmaceutical companies, the FDA and that ridiculous organization, the AMA are pushing statins for one reason…money. There is no money in correcting true risk factors.
Mike,
Last year at my physical for the first time my Dr. told me that my “bad cholesterol” was 258 and my “good cholesterol” had improved by a good amount. It was better than the previous year. High cholesterol runs in my family. His advice was to do nothing for now and see how my levels read the next time. I just had them done. I’m a bit nervous to get them back. I am definetly not a drug person. I used bioidenticals in moenpause without his support. I’m not sure where to go from here in a healty way. When I get my test results back maybe you could offer your advice.
LS
AB your responses are influenced by selective data.
New data from the TNT Study reveals that subjects who had their LDL-C levels substantially reduced with high dose Lipitor (80mg), nevertheless remained at risk if their HDL-C levels remained low. Peter Libbey et al showed that in all the major Statin intervention trials the subjects have remained at risk despite their lowered LDL-C levels (JAM.COLL.CARDIOL. 2005;46;1225-8) and in a meta-analysis of 90,000 subjects in 14 prospective randomized statin trials, low HDL-C at baseline represented a significant contributor to cardiovascular risk.(Lancet 2005, 366:1267-78)
The drug industry has woken up the fact that lives are not saved through statin induced LDL-C reduction, hence the frantic rush to produce HDL-C enhancing “chemicals”,which we know cannot be achieved by statins. Lifestyle changes and dietary modifications have been proven to increase HDL-C levels, and we as physicians are failing miserably in promoting these highly effective interventive strategies. We need to look at what we are doing in our consulting rooms and seriously ask ourselves, “are we doing harm…or are we promoting health?”
The AHA has failed to promote health-enhancing targets and still pushes the concept of low fat diets ! Evidence is abundant that good, healthy, saturated fats, as part of a diet incorporating flavenoids and carotenoids are able to improve healthy HDL-C levels, and many doctors are still failing to grasp this truth.
Mike states that the distinction between “good” and “bad” cholesterol is hilarious. He is absolutely correct, except that it is not only hilarious, but a sad commentary on our impoverished insight into human physiology, and a very dangerous and false interpretion that has confused , not only members of the public, but many practising doctors as well !
Thank you N. Wilson for your comments. The harm that has been done and continues to be perpetuated by the pharmaceutical and medical industries for the sake of money is unforgivable. The answers to improved health are out there. The simplistic view that cholesterol is the cause of heart disease is unacceptable. The continued marketing of the lipid hypothesis illuminates just how easily judgments can be skewed when large amounts of cash are at stake.
How many more lives are going to be ruined? How much farther can our food supply be pushed away from its original packaging? Not to single out doctors because there are some great docs, but what will it finally take to get the medical community to actually stand up for the health of their patients? Western medicine needs to get back to its roots as holistic healers with an emphasis on prevention. Real prevention backed by sound nutrition and honoring the connection between the emotional, spiritual and physical. Not just prevention through medication and the food pyramid.
N. Wilson thanks again for your comments. Keep blogging and getting god information out there.
Good post Mike.
Just like to add that normalising vitamin D is now recognised as a vital factor in the heart disease/inflammation scenario.
Dave,
You’re absolutely correct, and the pro-vitamin D evidence is stacking continuously. People who are diagnosed with cancer, heart disease or other illnesses are consistently found to be deficient in Vit D.