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Omega-3 Findings Point to Greater Cardiovascular Potential
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Landmark research reveals that omega-3s may help prevent and stabilize the arterial plaque that throws off heart attack- and stroke-inducing clots

by Craig Weatherby

Statins: Synthetic copies of an ancient Chinese remedy

Statins are synthetic drugs, but, like many drugs, simply copy a natural remedy. In this case, it was a yeast that grows on red rice, and drug companies noticed that Chinese researchers had already documented some of the positive cardiovascular effects of this traditional Chinese remedy.

Thanks to what many consider egregiously unjust U.S. laws paid for by big pharma, a pharmaceutical giant quickly patented the active compound, which made it immediately illegal to associate any statements – no matter how legitimate – about heart health with the sale of an ancient natural remedy.

Statins’ anti-inflammatory effects are similar to those exerted by omega-3s, aspirin (at risk of silent gastric bleeding), and the flavonoids abundant in colorful plant foods, cocoa, and tea.

According to the U.S. Centers for Disease Control and Prevention, heart disease is the number one killer of Americans and a major cause of disability.

And there’s little doubt that reducing atherosclerosis – plaque build up in the arteries – would reduce rates of fatal heart attacks or strokes significantly.

Omega-3s have been linked to reduced rates of stroke, second heart attack, and sudden cardiac death.

And until now, these benefits were attributed to two major factors: reduced triglyceride levels and reduced risk of arrhythmia's.

But new research adds key, inflammation-related explanations for the documented heart benefits of omega-3s:

  • Reduced inflammation in artery walls;

  • Enhanced healing of the routine arterial lesions that, left unhealed, promote plaque formation;

  • Reduction in the amount of lesion-induced arterial plaque (atherosclerosis);

  • Less chance that inflammation-related events will cause arterial plaque to rupture and cause a heart attack

Folks familiar with the medical literature know that the benefits associated with some statin drugs – reduced rates of heart attack and sudden death – have little to do with these compounds’ cholesterol-lowering effects.

While the statins that lower cholesterol levels the most also tend to be the best at reducing risk of adverse heart events, this link now appears to be more of a coincidental association than a compelling explanation for statins’ heart benefits.

In fact, overall, the links between cholesterol levels and heart risk are weak.

Instead, it’s increasingly clear that most heart attack risk stems from injury to our arteries – much of it induced by diet- and lifestyle-related “silent” inflammation – and that the preventive health benefits of statins stem primarily from their anti-inflammatory effects.

Chronic, “silent” inflammation results from starchy, sugary diets high in pro-inflammatory omega-6 fats from grain-fed meats and common vegetable oils (except olive oil, macadamia nut oil, and hi-oleic sunflower oil).

And arterial inflammation is discouraged by diets rich in omega-3s, tea, cocoa, and colorful, antioxidant-rich fruits and vegetables.

This so-called “sub-clinical” inflammation – which produces no overt symptoms and shows up only in sensitive blood tests – plays (at least) three key roles in promoting arterial plaque:

  1. Inflammation generates free radicals that oxidize cholesterol, which then accumulates in and damages artery walls (atherosclerosis);

  2. Inflammation causes blood cells and fats in the blood to become sticky and clot-prone;

  3. Inflammation destabilizes arterial plaque – which is full of oxidized cholesterol and blood cells – causing it to rupture and throw off artery-blocking clots that produce heart attacks, arrhythmias … and sometimes, sudden cardiac death

So the release of a credible study that put omega-3s at the center of arterial inflammation prevention and resolution sent serious tremors through the cardiovascular research community.

Omega-3s seen healing arteries injured by inflammation

New discoveries from animal studies conducted by scientists from Harvard and Texas confirm that arterial plaque (atherosclerosis) – and the heart-stopping artery blocks that result when arterial plaque ruptures – both result from inflammation gone awry.

Two related new studies further our understanding of dietary and genetic factors that promote or discourage atherosclerosis and resulting adverse heart events.

Both studies involved experiments in mice, but cover biological processes present in humans.

Study #1: Blocking a rogue protein could prevent arterial inflammation

In the first study, scientists from Boston's Brigham & Women’s Hospital and Harvard Medical School showed how an immune system protein called “ROCK1” greatly increases inflammation in the walls of blood vessels, which is provoked by atherosclerosis (fatty arterial plaque).

The scientists found that ROCK1 is necessary for the immune cells called macrophages to remove fatty deposits from vascular walls (Wang HW et al. 2008).

But macrophage cells also release pro-inflammatory chemicals, and swallow oxidized cholesterol and fats. This turns some of them into “foam cells”, which can scar or stick to the artery the cell was meant to clean, making matters worse.

Inflammation is a normal byproduct of the clean-up process and, when it goes unchecked, leads to clogging and hardening of the arteries.

When the researchers created mice that lacked ROCK1, the animals’ macrophages no longer contributed to these fatty deposits and the mice showed significantly less inflammation and atherosclerosis.

This discovery could lead to new treatments, such as ROCK1 inhibitors, that could dampen the inflammatory response to fatty deposits and slow the progression of atherosclerosis, and in so doing, reduce the incidence of heart attacks and strokes.

Study #2: Omega-3s needed to end inflammation and heal arteries

While the first study points to a protein that promotes inflammation, it remains to be seen whether any drug or food factor will be found that suppresses production of this agent, and whether that is a safe thing to do. (Deleting ROCK1 from mice kills most of them shortly after birth.)

The second report – funded by the American Heart Association and the National Institutes of Health – focuses on a more practical approach to arterial inflammation.

Researchers from Harvard and Houston’s Baylor College of Medicine examined how to prevent inflammation from running amok (Merched AJ et al. 2008).

Recently discovered agents called “lipid mediators” play key roles in regulating the body's ability (or inability) to dampen inflammation after the body’s artery clean-up machinery kicks into high gear.

These mediators – which include lipoxin A4, resolvin D1, and protectin D1 – are essential to putting a damper on damaging arterial inflammation, and to ending inflammation and allowing artery healing.

The major lipid mediators needed to dampen arterial inflammation are derived from the omega-3 fatty acids in fish, as described by the authors: “The biosynthesis of these local acting mediators is regulated by availability [in cell membranes] of fatty acid precursors such as omega-3 polyunsaturated fatty acids.”

And we can only get omega-3s into our cell membranes two ways: 1) by eating modest amounts of fatty seafood, or 2) by eating lots of green plants, grass-fed meats, and flaxseed.

In many instances, even in very young people, lesions (little sores) arise inside arteries and then resolve. The mystery is why some lesions do not heal.

What the Baylor-Harvard team found was that genetic manipulations of mice, which increased their production of inflammation-ending lipid mediators, gave the lesions a chance to heal or the atherosclerosis to slow down.

In contrast, genetically clamping down on these inflammation-ending signals fanned the fire of inflammation and sped up the progression of atherosclerosis.

According to lead author Dr. Aksam J. Merched, assistant professor at Baylor, “Inflammation is a two-edged sword. If resolution fails and the response gets out of hand there is a never ending civil war in the body. Continued inflammation draws more macrophages (immune system cells) to the site of the inflammation. They produce [pro-inflammatory] molecules that turn this into a vicious cycle.”

Baylor professor Lawrence C.B. Chan put it this way: “Resolution is not a passive process. It is active and produces specific anti-inflammatory mediators that ‘cool down’ the inflammatory process.”

By increasing levels of these lipid mediators and facilitating their production – such as by increasing dietary intake of omega-3s from fish and decreasing intake of pro-inflammatory omega-6s from vegetable oils and grain-fed meats – the scientists believe we can significantly reduce the inflammation that underlies much of atherosclerosis.

As the authors found, “Atherosclerosis is now recognized as an inflammatory disease involving the vascular wall. Recent results indicate that acute inflammation does not simply passively resolve as previously assumed but is actively terminated by a homeostatic process that is governed by specific [omega-3-derived] mediators...”

Things just keep looking better and better for omega-3s… and people who can get ample amounts into their diets.

For more on this topic, see “Inflammation, Cardiovascular Disease, and Omega-3s,” “Reverse Heart Disease Now: Dr. Sinatra’s New Book,” and “Omega-3s Seen Rivaling Statins at Reducing Risk of Death.


  • Baylor College of Medicine. June 18, 2008. Failure to bridle inflammation spurs atherosclerosis. Accessed online June 27, 2008 at
  • Chen Y, Wang J, Nie R, Zhou S. Endogenous pro-resolving and anti-inflammatory lipid mediators: The new hope of atherosclerotic diseases. Med Hypotheses. 2008 Apr 28. [Epub ahead of print]
  • Merched AJ, Ko K, Gotlinger KH, Serhan CN, Chan L. Atherosclerosis: evidence for impairment of resolution of vascular inflammation governed by specific lipid mediators. FASEB J. 2008 Jun 17. [Epub ahead of print]
  • Serhan CN. Lipoxins and aspirin-triggered 15-epi-lipoxins are the first lipid mediators of endogenous anti-inflammation and resolution. Prostaglandins Leukot Essent Fatty Acids. 2005 Sep-Oct;73(3-4):141-62. Review.
  • Serhan CN. Novel omega-3-derived local mediators in anti-inflammation and resolution. Pharmacol Ther. 2005 Jan;105(1):7-21. Review.
  • The FASEB Journal. New discoveries from Harvard and Baylor get to the heart of cardiovascular disease: atherosclerosis is inflammation gone awry. Accessed online June 27, 2008 at
  • Wang HW, Liu PY, Oyama N, Rikitake Y, Kitamoto S, Gitlin J, Liao JK, Boisvert WA. Deficiency of ROCK1 in bone marrow-derived cells protects against atherosclerosis in LDLR-/- mice.FASEB J. 2008 Jun 12. [Epub ahead of print]

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