For decades now, we have been told that fatness (or “obesity”) is a major cause of diabetes. Health “experts” have warned about this, but they could never say how being overweight could cause insulin resistance (IR). Without IR, you can’t have Type 2 diabetes, so the whole “blame fat” theory has been suspect.
Well, now they have a plausible explanation. Obesity may cause inflammation, causing IR, leading to diabetes. But is this theory true? Does adipose (fat) tissue really create inflammation? Or do both obesity and inflammation come from some other cause? Get ready for some science as I try to explore these questions.
In a new report in the Journal of Leukocyte Biology, two Japanese scientists report that “obesity is associated with a state of chronic, low-grade inflammation.” They explain that as fat cells get larger, they seem to attract immune cells called macrophages. These cells produce inflammatory chemicals called cytokines that help cause insulin resistance. Chief among these chemicals are interleukin-6 and tumor necrosis factor-alpha.
In animal models, insulin resistance doesn’t occur until after macrophages invade the fat cells. So the question remains, which comes first, the inflammation or the fatness? What draws the immune cells into adipose tissue?
Remember that most overweight people never develop diabetes. And some overweight people have much more inflammation than others. (The same is true of thin people, of course.) Why do some develop this fat-related inflammation and some don’t?
Some think that weight itself provokes inflammation. According to French scientists writing in the journal European Cytokine Network, weight loss is associated with reduced “macrophage infiltration” and reduced inflammation. Also, another chemical, adiponectin, protects against insulin resistance and blood vessel damage. Adiponectin levels are often reduced in obese people for some unknown reason.
But researchers at the University of Tennessee found that most of the inflammatory chemicals released by adipose tissue do not come from fat cells, but from other cells (probably the macrophages) that have invaded. The fat cells themselves produce more leptin and adiponectin, chemicals that should reduce insulin resistance.
What Is Going On?
Why should increasing the size of fat cells cause inflammation? Inflammation is the body’s response to a threat (like an infection) or an injury. I can’t see why fatness should cause this reaction.
One possible answer is stress. Microbiologist Paul Black, MD, at Boston University writes that “repeated acute or chronic psychological stress may cause [inflammation seen in diabetes and cardiovascular disease].” He thinks that it may be the combination of stress and increasing fat levels that leads to insulin resistance and diabetes.
In another paper, Dr. Black reported that the liver and fat tissues are two of the biggest sources of cytokines, and that stress often activates cytokine production. So it looks as though fatness creates a potential risk of inflammation (because fat can produce more cytokines), and stress may be the actual cause (by telling the fat cells to actually produce these chemicals.)
Of course, there are many causes of inflammation besides stress. And there are many causes of stress besides psychological stress. Cold, heat, infection, fatigue, pollution, certain chemicals, and many other factors can create stress and/or inflammation. Yet the “experts” are convinced that fat is the only significant cause. I doubt it.
Obviously, as the scientists like to say, more research needs to be done. But since sustained weight loss is so difficult, I think the priority for heavy people should be to reduce inflammation, not to lose weight. Reduce stress, take an anti-inflammatory like salsalate, take care of your gums. (Gum disease is a major source of inflammation.) Relax, get out in nature, things like that.
Note: I loved the outpouring of responses to the blog entry on reasons to live. I think it would be great to do a book on reasons to live. (I have a chapter on it in The Art of Getting Well, but I’d like to expand it into a book.) I could use your help. If you have any stories about reasons to live, the benefits of having them, or the effects of not having them, please send me an e-mail at firstname.lastname@example.org.