Volume11, Issue 19 March 5, 2014
How to overcome the damage belly
fat does to your arteries
You probably know that I have beaten the drum about metabolic syndrome and belly fat. I've told you how visceral fat (within your abdominal cavity) is associated with significant disease. Well, new research shows just how damaging this fat is to your arteries.

Researchers recently studied the different types of fat in mice. They developed genetically identical mice with one specific defect. They lacked a key fat metabolizing hormone called leptin. Fat makes leptin. It plays a role in appetite, metabolism, as well as reproduction. The researchers transplanted fat cells from normal mice into some of the mice. By chance, the scientists discovered that those receiving the transplant developed chronic inflammation. It concentrated around individual transplanted fat cells. Now that couldn't be due to their genetics, since all the mice were identical. It had to be due to the transplanted cells.

With this knowledge, the researchers turned to consider the link to atherosclerosis. Mice don't normally get atherosclerosis. So the researchers used another strain of mice genetically lacking a certain protein. These mice quickly developed the disease. They divided these mice into three groups. They transplanted visceral fat into one group. Then they transplanted subcutaneous fat - the type that's found just under the skin throughout the body - into another group.

Sure enough, the mice with the visceral fat transplants fast tracked to atherosclerosis. They got inflammation identical to the leptin-deficient mice that had the visceral-fat transplants. Interestingly, the mice that had the subcutaneous fat transplant didn't develop accelerated atherosclerosis. However, they did get increased inflammation. The researchers gave a third control group a "sham" operation. They didn't get inflammation or increased atherosclerosis. The conclusion? There is something specific within visceral fat that's strikingly different than all other fat.

Daniel Eitzman, MD is a cardiologist, laboratory scientist, and associate professor who led the study. He said that macrophage cells appeared in the visceral fat. These are highly inflammatory cells. They also invade your blood vessel walls in atherosclerosis. The presence of these cells in the visceral fat of the mice was highly related to their increased arterial disease. Blood vessels far from the site of the fat transplant developed increased atherosclerosis. Please read that last statement again. Visceral fat is synonymous with inflammation. And the inflammation of visceral fat promotes atherosclerosis far away from the fat.

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Finally, the scientists wanted to lock in their findings. They treated the transplanted mice with a drug that reduces diabetic inflammation. In the visceral fat transplants, it did reduce the number of macrophages. It also reduced a key biochemical inflammatory marker. It further reduced their atherosclerosis development. It didn't do these things for the subcutaneous fat transplants.

Moral of the story: The fat under your skin is not your problem. It's the fat in your belly and around your vital organs that is. It's a factory for inflammation and long-distance arterial disease. That is the essence of the metabolic syndrome, now epidemic worldwide. However, reducing inflammation with drugs is not the answer. There's only one answer. It's diet and lifestyle changes. And the one diet that I have not yet seen fail, when adhered to, is one where 70-80% of what you eat is fresh raw veggies and fruit. Of course, exercise to burn off the fat is part and parcel of the therapy. Atherosclerosis secondary to metabolic syndrome is an entirely preventable disease.

You also can help control systemic inflammation by using the supplement Reduloxin, which is one of the best anti-inflammatory supplements I've seen. It won't completely stop the impact of belly fat. But when you take it along with eating a healthful diet and plenty of exercise, it can help you avoid the damage belly fat causes.


Circulation, published in advance online January 22, 2008.

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