A New Culprit In Atherosclerosis?

An article entitled “A New Culprit in Atherosclerosis”, published on ScienceDaily.com on January 9th 2012, speaks about a new discovery in the search for a “cure” for Heart Disease.

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“We have discovered that macrophages that accumulate in plaques secrete a molecule called netrin-1,” said Kathryn J. Moore, PhD, senior author of the study and associate professor in the Departments of Medicine and Cell Biology at NYU Langone Medical Center. “Our study shows that netrin-1 blocks the normal migration of macrophages out of arteries, causing these immune cells to accumulate and promote the progression of atherosclerosis.”

Artery plaques that break off causing vessel blockages, or potentially fatal heart attacks and strokes are known to have high macrophage cell content. Atherosclerosis is fueled by the presence of these cholesterol-laden macrophages in the artery wall. Typically, the immune system sends macrophages to clean up cholesterol deposits in arteries, but once they fill up with the unhealthy form of cholesterol they get stuck in the arteries, triggering the body’s inflammatory response. The bloated

macrophages then become major components of plaque lining artery walls. Until now, the mechanism by which macrophages become trapped has remained unknown.

In this new study, researchers show why macrophages remain in artery plaques leading to atherosclerosis. Netrin-1 promotes atherosclerosis by retaining macrophages in the artery wall. In fact, netrin-1 signals macrophages to stop migrating and as a result these cells accumulate within the plaque. In addition, study experiments show, genetically deleting netrin-1 can minimize atherosclerosis, reduce the level of macrophages in plaque and promote the migration of macrophages from plaques.

“Our study identifies netrin-1 as a novel target for future therapeutic intervention for the treatment of atherosclerosis and cardiovascular disease,” said Janine M. van Gils, PhD, lead author of the study and a post-doctoral researcher in the Marc and Ruti Bell Vascular Biology and Disease Program, Leon H. Charney Division of Cardiology, Department of Medicine at NYU Langone Medical Center. “This discovery provides new clues to help reduce the amount of plaque in arteries and the threat of atherosclerosis, a major cause of mortality in Western countries. The development of a new strategy to diminish macrophage accumulation in plaque offers great promise to reducing the occurrence of fatal cardiac events.”

While I find this new discovery to be a positive thing, I still see it as another seemingly misguided attempt to “intervene” in to a process that has already begun, while neglecting to identify and eliminate the cause.

The macrophages don’t just hang around in the arteries for no reason. They’re not just all sitting around, having a fun little macrophage get together; they are there, because their job is to clean up dead stuff, which in this case is arterial plaque. Have these researchers really found a new culprit in atherosclerosis, or just another link in the chain? What causes the plaque in the first place? In my opinion, it’s the overabundance of fragile and easily oxidized polyunsaturated fatty Acids (PUFAs) in the Western Diet….or the S.A.D (Standard American Diet) as we call it…..that are the true cause of the plaque. The PUFAs induce inflammation and damage in the artery walls, creating tiny cracks in them that are just large enough to allow small and dense Lipoproteins to become trapped, and build up over time to form plaque deposits.

An easy way around this is simply to avoid as many unsaturated fats as possible. Saturated fat is our friend. Make sure that the majority of your fat intake is from animal sources, not plant sources, and you should be able to avoid plaque building up in your arteries. I don’t know that for sure, because no one does, but it sounds logical, doesn’t it? Let’s not forget that avoiding gluten-containing grains is a good idea too, and will definitely help avoid inflammation!


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8 Responses to A New Culprit In Atherosclerosis?

  1. Félix Boissonneault January 27, 2012 at 8:44 am

    Reminds me of Cancer. While I’m not a die-hard expert, like the macrophages, I know cancer is not an evil thing. It’s an evolutionary way our genetics have found to keep producing cells in a toxic environment in order for you to live a little longer (by creating new networks to bring oxygen). The fun thing is, if you find a way to restore this toxic frame, cancer will no longer have a reason to propagate and healthy cells shall populate once again. Yet all conventionnal medecine do is trying to inhibit your body’s last hope (with aggressive treatments like chimiotherapy, that is). Correct me if I’m wrong.

    • Barry Cripps January 27, 2012 at 11:01 pm

      Right……all of these drugs cover up the problem by putting a bandage on the symptoms, but they never fix the root of the problem. And yes, sometimes the “fix” causes more problems than the original disease.

  2. Maeve January 27, 2012 at 12:04 pm

    What, then about olive and coconut oils?

    • Lila Solnick January 27, 2012 at 1:37 pm

      Hi Maeve,

      Olive is okay in moderate amounts. It probably shouldn’t be the main fat that you use, and probably wouldn’t be because cooking in olive oil is not really a good idea. It can get damaged easily by heat. It’s great for dressing and added to cooked dishes for flavor. One thing that I like to do is make sun butter. It is a combination of olive oil and butter. It’s really good on mashed cauliflower.

      Coconut oil, on the other hand, is a fantastic oil. It is my primary oil. I use expeller-pressed coconut oil for cooking and virgin coconut oil for everything else, including the 4 tablespoons that I take each day. I use so much coconut oil that I buy the virgin oil by the gallon. I also use it on my skin so a lot gets used. Plus because it is a saturated fat it does not go rancid. That gallon may last 6 - 8 months, even during the hottest weather, but it’s still good!

      Thanks for commenting

  3. Lyndsey January 27, 2012 at 7:27 pm

    What drives me nuts is that no one addresses why LDL adheres to vessel walls. “they” make it sound like it just randomly happens if your LDL is high. I can not believe that LDL adherence to epithelials “randomly, just because there is too much LDL particles” is the beginning of atherogenesis. Regardless, this study was done on mice that had to be fed a “Western diet” for 12 weeks to build some atheromas and screw the body up before they could test gene deletion.

    • Barry Cripps January 27, 2012 at 11:00 pm

      You’re right Lindsey. It’s a fundamental breakdown in logic…..I don’t understand it either.

  4. Dan January 28, 2012 at 3:05 pm

    Once again another great read!!!!! I totally agree too they seem to be doing the same thing as they did with cholesterol - the macrophages seem to be there because they are trying to help.

    The old story of correlation does not equal causation. But I guess that doesn’t get funded.