Fish oil (dha plus epa) works better than statins at improving hdl cholesterol
Fish Oil (DHA plus EPA) Works Better Than Statins at Improving HDL Cholesterol
A study has shown that fish oils are more effective than the statin drug Lipitor in positively affecting the levels of HDL ("good") cholesterol in obese and insulin-resistant people. HDL cholesterol protects against atherosclerosis by removing excess cholesterol from arterial cells, and low HDL levels can therefore increase the risk of cardiovascular disease, particularly for those who are obese and/or insulin resistant.
In the six-week study, fish oils and Lipitor were given to 48 men, both separately and combined. Fish oil and Lipitor together greatly lowered plasma triacylglycerols and raised HDL cholesterol levels.
But fish oil alone also influenced HDL cholesterol by altering the production and catabolism rates of HDL apolipoproteins (catabolism is the breakdown of complex molecules metabolically into simpler ones). Lipitor did not increase this effect when combined with the fish oils, and did not produce a similar effect on its own. July 2006; 84(1): 37-43 Comment:
The omega-3 fats in fish oil will influence HDL cholesterol levels far more safely and effectively than prescription pills -- and that for a fraction of the cost, typically even less than the copayment to purchase the expensive medications.
from selling Lipitor, which is up 11% from last year. A 30 day supply of the 10 mg pill is $90 while the 20 mg is $130. Of course anyone with half a brain who was taking the 10 mg could get a 20 mg dose, cut it in half lowering the drug bill by almost 30%, but since most of the drug bill is paid by insurance companies anyway, very few people do this.
Lipitor1) is not only less effective and more costly than the omega-3 fatty acids, but it stands also a good chance of depressing the patients immune system2) and even increasing their overall risk of atherosclerosis3) by raising Lipoprotein (a).
Statin drugs like Lipitor may treat one symptom by lowering LDL ("bad") cholesterol levels, but they do nothing whatsoever to treat the underlying disease, which is causing the problem in the first place. That's the same as putting a band-aid on an infected wound -- it might stop the bleeding, but it won't solve the actual problem. And, in addition to doing no good, they also actively cause harm. Statins kill people -- lots of people -- and they wound many, many more.
For example, taking statins eventually depletes important Coenzyme Q10 levels by blocking the body’s natural production mechanisms in the liver. This can lead to fatigue, muscle weakness, soreness and ultimately to heart failure.
So why risk health by using drugs when there are very simple things one can do to normalize cholesterol levels?
is one important tool that may reduce the risk of heart disease, as it effectively addresses one of the primary reasons why nearly everyone's cholesterol becomes inappropriately elevated, and that is elevated insulin levels.
One can also lower insulin levels by eliminating sugar and grains. Grains rapidly break down to sugars that will increase insulin levels. And, for most people with high cholesterol levels, the primary reason is high insulin levels. This approach normalizes cholesterol levels in nearly everyone -- unless they have a genetic defect called familial hypercholsterolemia.
Eliminating sugar and grains will also normalize weight, increase energy, lower blood pressure and triglycerides as well. Many helpful tips and recipes about this topic can be found in the book, Insulin: Our Silent Killer.
And, as the study above indicates, that is chock full of beneficial omega-3 fatty acids. To really enjoy all the benefits these oils have to offer, it's important to find one that has been independently tested in a laboratory and conforms to strict purity guidelines (ensuring that the oil is free from toxins like Mercury and Cadmium).
1) Lawsuits Debate Lasting Lipitor Damage
Two lawsuits have been filed against drug manufacturer Pfizer, Inc. claiming its cholesterol-lowering drug Lipitor caused lasting muscle damage -- and the company didn't adequately inform the public about the potential side effects.
The men behind the separate lawsuits both said they experienced debilitating pain, weakness and memory problems after taking Lipitor, a statin drug. The symptoms subsided after the drug was stopped, but pain, fatigue and a tingling sensation in the hands and feet still remains, one of the men said.
Pfizer maintains that the number of Lipitor users who experience such symptoms is well under 1 percent, and that the potential side effects are included on the drug's labeling and in advertisements.
Lipitor is the best-selling medication in the world and generates over $12 billion a year for Pfizer.
June 8, 2006 2) Lipitor May Suppress Immune System
Lipitor, Mevacor and Pravachol have been found to suppress certain immune system cells known as helper T-cells, according to new research from Switzerland.
The researchers and subsequent media reports have focused on the fact that the drugs may be useful for treating transplant patients. However, how this immune suppression could affect the vast majority of patients taking the drugs is not discussed.
"This unexpected effect provides a scientific rationale for using statins as immunosuppressors, not only in organ transplantation, but in numerous other pathologies as well," the researchers conclude.
Researchers found that in laboratory-grown cells, the statin drugs suppressed the activation of helper T-cells. T cells, of which there are 4 types, are a group of lymphocytes produced in the thymus gland. The four types are:
• Helper T cells • Killer T cells • Suppressor T cells • T4 cells Helper T cells, the type suppressed by the statin drugs, act by recognizing foreign pathogens and then activating the production of the proper T- and B-cells in response.
The statin drugs used in the study included the following:
• Lipitor™ (atorvastatin) • Mevacor™ (lovastatin) • Pravachol™ (pravastatin) Nature Medicine December, 2000; 6: 1311-1312, 1399-1402 3) More Reasons to Avoid Statin Drugs / Does Lipitor Raise Lp(a)?
Lipoprotein (a), or Lp(a), consists of an LDL particle covalently attached to apolipoprotein (a). In numerous studies elevated plasma levels of Lp(a) are positively associated with increased risk of atherosclerosis, myocardial infarction and stroke. There are experts who believe Lp(a) may even be the single most
important lipid in assessing one’s true risk of developing these conditions. Some researchers have established a genetic link to Lp(a) levels. It is synthesized in the liver.
Jim Ehmke, an experienced clinical nutritionalist, has been testing Lp(a) levels in his patients for at least the past six years. During this time he observed repeatedly that statin drugs - especially Lipitor - raised Lp(a) above the medical reference range.
His first “anecdotal” experience in this regard occurred, when he was testing his mother's lipids. At the time she was not taking statins and had just been diagnosed with atherosclerosis. Her initial Lp(a) was 26 with a reference range of 0 to 30. Although technically within range, he knew from many publications, that anything over 10 should be scrutinized. Against his advice his mother - being of the old school - went along with her doctor and decided to take Lipitor. Six months later he retested her Lp(a) and it was 76! Needless to say he was shocked and perplexed. After expressing his reservations to her physician he was not surprised to learn, that the doctor knew absolutely nothing about Lp(a).
After this experience he began to check Lp(a) on as many patients as possible with special interest to test Lp(a) levels before and after statin use. To his amazement, after three months on Lipitor, a very high percentage of patients who had normal levels of Lp(a) before taking Lipitor, had elevations above the reference range. He kept scratching his head thinking, "Could it be that Lipitor actually worsens heart and artery disease? That the very thing touted to reduce such risks could actually increase them? Is vital information on this huge moneymaker being withheld?"
Obviously, this is not proof of anything, just an interesting observation. Perhaps some other clinicians have already observed something similar--or not. If this is a valid anecdote, as my experience suggests, the grass roots efforts of practitioners in the field could conceivably lead to the funding of a larger study to prove or disprove the possibility that Lipitor raises Lp(a). If the tens of millions of people who take Lipitor every day are actually harming themselves, it would be a worthy public service to reveal this fact.
Lastly, in discussions with various lipid specialists, including the head of a lipid department at a major university, it was learned that a pharmaceutical version of niacin - called Niaspan - is very effective at reducing Lp(a). So in those cases where it is necessary to lower Lp(a) there is the option of using Niaspan. Plus, because Niaspan cannot be patented, it costs a fraction of what statin drugs cost. No wonder it's not marketed aggressively.
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