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Silent Killer: The Link between Obesity and Type 2 Diabetes

Share This article Obesity is one of the biggest generators of silent inflammation. Since nearly two-thirds of Americans are now overweight, this means that the epidemic of silent inflammation is also out of control. By the same token, our diabetes epidemic has grown by 33 percent in the last decade. It should come as no surprise that all three epidemics have worsened in recent years. All three are intricately connected with a condition known as insulin resistance.

Insulin resistance occurs when your cells become less responsive to the actions of insulin, forcing your pancreas to continuously produce more insulin to drive glucose into cells. This excess insulin (produced as that response to insulin resistance) also increases the storage of body fat. So the real question behind our current obesity epidemic is what actually causes insulin resistance?

No one knows for sure, but there is a growing opinion that the molecular cause of insulin resistance may originate in the endothelial cells. Endothelial cells form a very thin barrier that separates the bloodstream from your organs. If this barrier is not working very well, you have a condition called endothelial dysfunction, which means among other things that insulin can no longer easily pass from the bloodstream through the endothelial barrier to interact with its receptors on the cell surface. It’s only when insulin interacts with these receptors that the cell can take up glucose from the bloodstream. Any difficulty insulin has in getting to its receptors will keep blood glucose levels elevated. The body responds by pumping out still more insulin, now creating a condition known as hyperinsulinemia.

Obesity from a Different View
What if the epidemic rise in obesity in the last twenty years was not primarily due to the usual suspects (fast food, TV, junk food), but fueled by increased silent inflammation, which increases insulin resistance? This means that unless you reduce the underlying silent inflammation, any other approach to reduce obesity may be doomed to failure. This also means that simply restricting calories will not be enough to turn back our current obesity epidemic.

I believe that obesity starts with excess arachidonic acid (AA). (Click here to read more about Arachidonic Acid.) You can increase arachidonic acid in the bloodstream either directly by eating too much of it (it’s particularly high in fatty red meats and egg yolks) or indirectly by consuming too many high glycemic-load carbohydrates, which increase insulin production, which in turn promotes increased AA production. Either way, the body goes to great lengths to take any excess AA out of the circulation and store it away in your fat depots in an effort to keep inflammation under control.

Here is where the trouble starts, because fat cells aren’t simply inert balls of lard sitting on our stomach, thighs, and hips. These cells are very active glands that can secrete out large amount of inflammation mediators if they’re given the right stimulus. As your fat cells become filled with more AA, it causes an overproduction of pro-inflammatory eicosanoids in the adipose (fatty) tissue.

Eicosanoids play an integral role in your health. Just ask the Nobel Prize committee, which awarded the 1982 prize in medicine for the discovery of eicosanoids. They are also the most powerful hormones, since they affect the synthesis of virtually every other hormone in your body. In a sense, you can think of eicosanoids as “super-hormones” capable of bringing great health benefits (“good” eicosanoids), or great harm (“bad” eicosanoids), depending on which one a cell produces.

Now you can probably guess what happens. These “bad” eicosanoids induce the formation of new inflammatory mediators that spew forth from fat cells into the surrounding circulation--and generate systemic silent inflammation.

Now before you start cursing all your fat, I want to emphasize that all fat is not created equal. Some types of fat are far more harmful than others. It depends on their metabolic activity. Subcutaneous fat--the fat that collects on your hips, thighs, and buttocks and makes you look like a pear--isn’t that harmful. It may not look too good, but at least it won’t kill you, because your body is in no rush to mobilize the AA out of these fat cells. That’s why this type of fat is considered metabolically inactive. It is primarily a storage depot.

On the other hand, visceral fat can be a killer. This kind of fat collects around the abdominal organs, such as the liver, kidneys, and gallbladder and makes you look like an apple.

How do I spot visceral fat?
You may think that the easiest way to see if you have visceral fat is to look at yourself in a mirror. But this may be deceptive, because visceral fat is often found with in close contact with subcutaneous fat in the abdominal region. The real indication of the amount of your abdominal fat that is actually visceral fat is measured by either your TG/HDL ratio or your fasting insulin levels.

Visceral fat is very metabolically active and causes the constant release of stored AA into the bloodstream. This is the last place you want excess AA, since it’s then taken up by every one of your sixty trillion cells, making each one more likely to generate more pro-inflammatory eicosanoids, and therefore more silent inflammation throughout the body.

Visceral fat is even more insidious because it also continually releases other inflammatory mediators in addition to stored AA. Two of the worst are the pro-inflammatory cytokines, tumor necrosis factor (TNF), and interleukin-6 (IL-6). TNF is implicated in creating even more insulin resistance, whereas IL-6 triggers the liver to synthesize C-reactive protein (CRP), which can stimulate your white blood cells to begin to mount an inflammatory response to a potential infection (even though there isn’t one). About a third of the CRP circulating in your blood came directly from visceral fat cells. These pro-inflammatory cytokines are produced in your visceral fat as a response the increased pro-inflammatory eicosanoid production caused by increased AA levels.

This means the fatter you are (really, the more visceral fat you have), the more silent inflammation you generate. This is the smoking gun that links obesity with increased rates of heart disease, cancer, or Alzheimer’s. Anything that increases silent inflammation is going to be bad for your future.

Can you be fat and healthy?
Surprisingly, the answer is yes--but with a few caveats. You can be overweight and in a state of wellness if you keep your levels of silent inflammation under control. Since obesity generates inflammation, you may have to take more fish oil than the average person to reverse the silent inflammation induced by it. While losing weight is slow and hard, reducing silent inflammation using Ultra Refined high-dose fish oil is rapid. How much Ultra Refined high-dose fish oil do you need? This depends on your diet. If you are following the Zone Diet, you might only need to take 5 grams of EPA and DHA per day. If you follow the typical American (very high glycemic-load) diet, you’ll need to increase your dosage of Ultra Refined high-dose fish oil to a higher level.

Remember, all the medical complications of obesity come from the inflammation it generates. Ultra Refined high-dose fish oil is an immediate antidote to that inflammation.

Keep in mind being fat and healthy can be a dangerous game to play. It’s a little like lighting a cigarette with a stick of dynamite. You can do it, but you have to be very careful. The day you stop taking adequate levels of Ultra Refined high-dose fish oil is the day your silent inflammation will return, accelerating you toward chronic disease and faster aging. As long as you keep your Silent inflammation Profile under control, the likelihood of maintaining your wellness is pretty good in spite of your weight.

The one-two punch of silent inflammation and increased hyperinsulinemia caused by insulin resistance if left unchecked can lead to one of the most costly of chronic diseases: diabetes.

The Diabetes Connection
Diabetes used to be a very rare disease, but times have changed. Over the last twenty years, it has become an epidemic. Okay, let me clarify this. Type 2 (adult-onset) diabetes has become an epidemic, while type 1 (juvenile) diabetes still remains relatively rare. Type 1 diabetes is caused by a condition in which the pancreas completely shuts down and fails to produce any insulin, causing blood sugar levels to spiral upward out of control. The more common type 2 (90 percent of all diabetics have this version) occurs when the patient develops long-term insulin resistance. As I mentioned above, insulin resistance causes the pancreas to secrete more insulin (hyperinsulinemia) in an effort to reduce blood glucose levels. Eventually the pancreas (really the beta cells in the pancreas) just get tired and stop producing enough excess insulin. This is called beta-cell burnout. The result is that without enough insulin becoming secreted by the pancreas, blood glucose levels begin to raise to dangerous levels. The danger comes from two factors; (a) excess glucose in the blood produces free radicals (oxidative stress), and (b) excess glucose is neurotoxic to the brain. Hyperinsulinemia usually precedes the development of type 2 diabetes by about eight years, but they both come from increased insulin resistance. Starting to see the connection?

Obviously, not everyone who is has insulin resistance becomes a type 2 diabetic. However, enough do--there are an estimated 16 million Americans afflicted with type 2 diabetes. This devastating disease puts a person at a 2 to 4 times greater risk of dying from heart disease and also increases the likelihood of kidney failure, blindness, impotence, and amputation. Because of these expensive complications, type 2 diabetes is the most expensive of all chronic diseases, costing approximately $132 billion per year. As our obesity epidemic increases, so will the epidemic of type 2 diabetes. That’s very bad news for the health care industry.

The good news is that taking Ultra Refined high-dose fish oil to reduce silent inflammation (the molecular cause of insulin resistance) and following the Zone Diet will help reduce hyperinsulinemia (the consequence of insulin resistance) and begin to reverse type 2 diabetes in just six weeks.

Excerpted from The Anti-Inflammation Zone - Reversing The Silent Epidemic That's Destroying Our Health. Copyright 2005 by Barry Sears, Ph.D. Used by permission.

*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. As with any natural product, individual results will vary.

For more information about Dr. Barry Sears, his incredible fish oil supplements, or the popular Zone Diet, please visit

If you purchase any Zone Labs, Inc. products, part of the proceeds support CBN ministries.


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About The Author


Dr. Barry Sears is a leader in the field of dietary control of hormonal response. A former research scientist at the Boston University School of Medicine and the Massachusetts Institute of Technology, Dr. Sears has dedicated his efforts over the past 25 years to the study of lipids and their inflammatory role in the development of chronic disease. He holds 13 U.S. Patents in the areas of intravenous drug delivery systems and hormonal regulation for the treatment of cardiovascular disease.