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Does Fish Oil Lower Cholesterol? Does it Matter?
1/29/2007
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Common question misses the cardiovascular point: Omega-3s raise “good” and “bad” types alike, so their heart benefits stem from different effects

by Craig Weatherby



The short answer is "yes", but we need to qualify that statement.


The omega-3s in fish oil do not work like statins, which selectively lower only one kind of "bad" cholesterol, called LDL.

And the characterization "bad" cholesterol is a gross oversimplification of the ways in which cholesterol impacts cardiovascular risks.

It’s believed that the omega-3s in fish fat reduce the risk of strokes, sudden cardiac death, and second heart attacks by doing four things:

  1. Lower blood triglyceride (fat) levels.
  2. Raise levels of “good” (HDL) cholesterol.
  3. Lower levels of all non-HDL cholesterol
  4. Reduce risk of arrhythmias (conditionally, and not consistently)

We should note that fish oil can raise levels of LDL cholesterol slightly in people with high blood levels of triglycerides.


However, that otherwise slightly negative impact is insignificant when seen in the context of all of the effects that omega-3s exert on blood fats, blood cholesterol, arterial inflammation, blood stickiness (platelet aggregation), and other relevant risk factors for cardiovascular disease... such as the ability of omega-3s to lower levels of lipoprotein lipase, which traps LDL cholesterol in artery walls.

The skinny on cholesterol and cardio risk
Remember that when doctors talk about types of cholesterol such as LDL and HDL, they are really talking about different lipoprotein “packages” in which cholesterol is carried.


The body uses high-density lipoproteins (HDLs) to remove cholesterol from the blood, and it uses various kinds of low-density lipoproteins (LDLs) to carry cholesterol through the blood.


Having high levels of HDL cholesterol is good for cardiovascular health, but it is critical to understand that having “high” levels of LDL cholesterol is not inherently unhealthful.


In fact, the statistical links between LDL levels and heart risk are weak, with many persons dying from heart disease despite having “low” cholesterol levels, and vice versa.


Instead, the arterial plaque-buildup that defines arteriosclerosis and resulting cardiovascular disease gets created when LDL and other low-density carriers of cholesterol become oxidized by free radicals.


And those free radicals result from inflammation in the artery wall and blood.


This is why researchers at the National Institutes of Health (and around the world) increasingly point to excessivehence, pro-inflammatory, artery-irritatingintake of omega-6 fatty acids as the true nutritional cause of cardiovascular disease.


(Omega-6 fatty acids abound in common vegetable oils, the packaged and prepared foods made with these oils, and in grain-fed meats, poultry, and farmed fish.)


Of course, other factorsprimarily stress, sedentary lifestyles, diets high in empty calories, and genetic profilesalso play major roles in cardiac risk.


How omega-3s affect cholesterol
Omega-3s do not “lower cholesterol” in the way that statin drugs (e.g., Lipitor)
which lower LDL cholesterol levels very substantiallyare designed to do.


In fact, omega-3s often raise levels of LDL cholesterol slightly in people with high triglyceride levels. But, for the reasons we just explained, this is not in itself a cause of concern.


Omega-3s tend to lower levels of all non-HDL types of cholesterol.


This effect of omega-3s is very significant, for three reasons (Bays H 2008; Bays HE et al. 2008):

  1. Non-HDL cholesterol includes all of the cholesterol carried by oxidation-susceptible—hence, plaque-promoting—lipoproteins, not just LDL.
  2. Having high blood levels of all non-HDL cholesterol predicts risk of arteriosclerosis better than high LDL levels alone do.
  3. After LDL-lowering treatment goals have been reached, reduction of total non-HDL cholesterol is a recommended secondary treatment target in patients with high blood triglyceride levels (200 mg/dl or more).

Cholesterol and cardiovascular health: exploding common myths
Back in 1984, the National Institutes of Health issued a “consensus statement” on heart disease, in which the agency advised the American public that the best way to prevent heart disease was to reduce their consumption of cholesterol levels and saturated fats.


In fact, while there was no such scientific consensus, there were mountains of evidence to the contrary.


Most folks are surprised to learn that many people with “unhealthy” cholesterol levels never suffer from heart attacks or die from cardiovascular disease, while the reverse is also true: that is, many people with low cholesterol levels have cardiovascular disease and/or die from sudden cardiac death.


While people are somewhat more likely to have a heart attack when they have one of three “cholesterol profiles”1) very high total cholesterol levels, 2) high levels of small, dense LDL cholesterol (which can imbed in artery walls more easily), and 3) high levels of oxidized LDLthe connection between total cholesterol levels or cholesterol profiles and adverse cardiovascular events or cardiac deaths is much weaker than we’re led to believe.


Triglyceride levels, blood stickiness (platelet activation), and vulnerability to arrhythmias are equally powerful predictors of the risks of heart attacks, sudden cardiac death, and strokes… and fish oil is proven to reduce all of these risk factors substantially.


In addition, insulin and leptin resistance and high triglyceride levels appear to rival cholesterol levels as predictors of cardiovascular risk, while inflammation, impaired immune-cell response to arterial plaques, and homocysteine levels are also key factors.


Most of the cholesterol in the blood comes not from foods, but from the liver, where it is created in response to signals from the body: signals influenced by dietary fats and many other factors.


Dietary cholesterol and saturated fats are not inherently artery-clogging substances, but both become problematic in the context of the average American diet, which is imbalanced deeply in key respects:

  • A low ratio of omega-3 to omega-6 fatty acids (see “New Report Finds Americans Need Far More Omega-3s”)
  • High sugar-starch intake
  • Insufficient intake of foods high in heart-protecting fibers, vitamins, minerals, and the polyphenol antioxidants abundant in tea, cocoa, and colorful fruits, vegetables, and wild salmon. (Salmon’s red-orange color comes from astaxanthin [ass-tuh-zan-thin]: a uniquely powerful carotene-class polyphenol antioxidant.)

The vast preponderance of evidence indicates that the heart disease epidemic afflicting Americans has little to do with their intake or blood levels of cholesterol.


Instead, the evidence points to the American diet’s dearth of anti-inflammatory, anti-arrhythmic omega-3s and wildly excessive intake of pro-inflammatory omega-6 fatty acidsfrom cheap vegetable oils (corn, soy, safflower, cottonseed, canola) used in home and restaurant cooking and in packaged foodstrans fats (from hydrogenated oils), sugars, and refined corn and wheat starches.


The reason why high blood levels of “good” HDL cholesterol are the newest measure of heart-health is that HDL cholesterol spirits excess LDL cholesterol out of sticky blood, thereby keeping it from being oxidized and/or sticking to arterial lesions.


And arterial lesions are also caused in large part by the chronic lack of dietary omega-3s and excess of dietary omega-6 and trans fats: an imbalance that promotes wear-and-tear damage to arteries, plaque build-up, and clot formation.


Statins and cardiac risks

If high total and LDL cholesterol aren’t the real problem, why are statinsinvariably described as “cholesterol-lowering” agentsthe leading heart drugs of today?


Despite the conveniently simple “cholesterol-lowering” label applied to statins, researchers agree that most of these agents’ cardiac risk-reduction effects do not flow from their power to lower cholesterol by blocking internal creation of cholesterol.

Instead, the benefits of statins drugs derive from their anti-inflammatory and anti-clotting effects, and from their beneficial impacts on endothelial (artery lining) function (Patel TN et al 2007, Stoll G and Bendszus M 2006).


As we’ve described in previous articles, omega-3s appear to have comparable life-preserving power. (see “Does Statins' Super-Star Status Make Sense?” and “Omega-3s Seen Rivaling Statins at Reducing Risk of Death”.)


Two years ago, German researchers published their review of 97 clinical trials, and came to this conclusion: “Statins and n-3 fatty acids [omega-3s] are the most favorable lipid-lowering interventions with reduced risks of overall and cardiac mortality.” (Studer M et al 2005)


As we reported, the review showed that statins hold a clear edge with regard to preventing first heart attacks, which omega-3s are not proven to prevent significantly.


However, the review found that omega-3s reduce heart-related deaths about as effectively as statins:

  • Omega-3s reduce the risk of sudden cardiac death – the cause of half of all heart-related deaths.

  • Omega-3s cut the risk of second heart attacks and consequent death or disability substantially.

The reviewers also found that omega-3s decrease the risk of death from all causes, almost as much as statins.


Although adverse liver and muscle effects from statins are relatively rare, these drugs reduce the liver’s production of coenzyme Q10: a key nutrient for muscle-heart health and mitochondrial (energy-producing) functions in all cells.


While tests do not show that statin therapy reduces blood or tissue levels of CoQ10 or mitochondrial function consistently, researchers haven’t conducted tests that reflect high, real-world statin doses or look in the tissues most affected by statins (Hargreaves IP et al 2005).


We do NOT suggest that you should ignore a doctor’s advice to take statins. We DO suggest that you read up on statins and the weakness and complexity of the links between cholesterol levels and cardiac risks before you take the advice blindly.



Sources

  •  Belk EM, Lichtenstein AH, Chung M, Kupelnick B, Chew P, Lau J. Effects of omega-3 fatty acids on serum markers of cardiovascular disease risk: a systematic review. Atherosclerosis. 2006 Nov;189(1):19-30. Epub 2006 Mar 10. Review.
  • Bays H. Rationale for prescription omega-3-acid ethyl ester therapy for hypertriglyceridemia: a primer for clinicians. Drugs Today (Barc). 2008 Mar;44(3):205-46.
  • Bays HE, Tighe AP, Sadovsky R, Davidson MH. Prescription omega-3 fatty acids and their lipid effects: physiologic mechanisms of action and clinical implications. Expert Rev Cardiovasc Ther. 2008 Mar;6(3):391-409. Review.
  • Bucher HC, Hengstler P, Schindler C, Meier G. N-3 polyunsaturated fatty acids in coronary heart disease: a meta-analysis of randomized controlled trials. Am J Med. 2002;112:298-304.
  • Davidson MH. Mechanisms for the hypotriglyceridemic effect of marine omega-3 Fatty acids. Am J Cardiol. 2006 Aug 21;98(4 Suppl 1):27-33. Epub 2006 May 26.
  • Happy and Hearty Fish Findings; Salmon use Magnetic Maps; FREE Sockeye Salmon or Sockeye Salmon Oil; Rosemary Roasted Salmon
  • Hargreaves IP, Duncan AJ, Heales SJ, Land JM. The effect of HMG-CoA reductase inhibitors on coenzyme Q10: possible biochemical/clinical implications. Drug Saf. 2005;28(8):659-76. Review.
  • Herman AG. [New insights into the etiopathogenesis of atherosclerosis and atherothrombosis] Bull Mem Acad R Med Belg. 2006;161(3-4):213-25; discussion 226-7. Review. French.
  • Jans DM, Martinet W, Van De Parre TJ, Herman AG, Bult H, Kockx MM, De Meyer GR. Processing of amyloid precursor protein as a biochemical link between atherosclerosis and Alzheimer's disease. Cardiovasc Hematol Disord Drug Targets. 2006 Mar;6(1):21-34. Review.
  • Nordoy A. Statins and omega-3 fatty acids in the treatment of dyslipidemia and coronary heart disease. Minerva Med. 2002 Oct;93(5):357-63. Review.
  • Patel TN, Shishehbor MH, Bhatt DL. A review of high-dose statin therapy: targeting cholesterol and inflammation in atherosclerosis. Eur Heart J. 2007 Jan 22; [Epub ahead of print]
  • Schrijvers DM, De Meyer GR, Kockx MM, Herman AG, Martinet W. Phagocytosis of apoptotic cells by macrophages is impaired in atherosclerosis. Arterioscler Thromb Vasc Biol. 2005 Jun;25(6):1256-61. Epub 2005 Apr 14.
  • Stoll G, Bendszus M. Inflammation and atherosclerosis: novel insights into plaque formation and destabilization. Stroke. 2006 Jul;37(7):1923-32. Epub 2006 Jun 1. Review.
  • Studer M, Briel M, Leimenstoll B, Glass TR, Bucher HC. Effect of different antilipidemic agents and diets on mortality: a systematic review. Arch Intern Med. 2005 Apr 11;165(7):725-30. Review.


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