Diabesity
And, what you can do about it.
There is a relatively new but very timely term to describe the obesity epidemic and its relationship to the Type 2 Diabetes crisis affecting people of every age: Diabesity.
Dr Francine Kaufman MD explains the roots of diabesity quite simply:
"Our ancient genes and our modern environment have collided. Our bodies store excess calories as fat. In ancient times calories were hard to come by. Today, fast food and junk food are everywhere. Coupled with our increasingly inactive lifestyle, the result is obesity”.
Damaging characteristics of our modern lifestyle
Dietary toxins including refined wheat, fructose (high fructose corn syrup), and industrial seed oils
Excessive carbohydrates (all carbs turn to glucose)
Environmental toxins (chemicals like Bisphenol A, pesticides, phthalates, flame retardants, and heavy metals)
Micronutrient deficiencies (especially magnesium and vitamin D)
Chronic stress (emotional, psychological, physiological);
Altered gut microbiota (caused by antibiotic use, poor diet, formula-feeding during infancy);
Sedentary lifestyle
Inflammation and Immune Response
Diabesity is characterized by chronic, low-grade inflammation and continuous stimulation of the innate immune system. The inflammation that accompanies diabesity is not associated with infection or other traditional signs of autoimmunity and seems to have its own unique features. Both inflammation and obesity are strongly associated with type 2 diabetes (T2DM).
The innate immune system defends us from infection or foreign substances in a non-specific manner. It’s our first line of defense against anything the body perceives to be harmful. The innate immune system’s primary response is inflammation. Normally inflammation is temporary and the body returns to homeostasis on its own. In autoimmunity, however, the body mounts a response against its own cells and tissues and becomes stuck in a perpetual loop of chronic inflammation.
Genetics do Play a Role
Our genetics may help explain why some individuals and populations are more likely to develop diabesity when exposed to a modern, western lifestyle. The evidence suggests, however, that even those with a genetic predisposition to diabesity do not become “diabese” unless they are also exposed to the environmental factors listed above. On the other hand, inflammation nearly always accompanies both obesity and diabetes. Notice that inflammation alone directly contributes to every single metabolic dysfunction associated with diabesity: leptin resistance, impaired fat, and glucose metabolism, insulin resistance, and beta-cell destruction. Inflammation can be considered the primary mechanism through which the modern lifestyle and genetics cause diabesity.
Type 2 Diabetes
This disease is an autoimmune, inflammatory disorder triggered by modern lifestyle, influenced by genetics, and characterized by impaired glucose and fat metabolism and fat hormone resistance. Most of us know that Diabetes impairs glucose metabolism. Diabetes also involves impaired fat metabolism. In healthy people, Free Fatty Acids are burned in the mitochondria soon after release (lipolysis) from stored forms of fat (triglycerides and phospholipids). In the diabese, inflammation, leptin resistance, and oxidative damage impair the mitochondria’s ability to burn fats. The excess FFAs then “spillover” into non-fat tissue like the liver, pancreas and skeletal muscles. These metabolically active tissues are damaged by FFA’s because they don’t belong there. This is called lipotoxicity. Several studies show that lipotoxicity causes insulin resistance and increases the risk of T2DM.
Hormonal Influence
Why is Leptin important? It is a hormone produced by body fat. It tells the brain to decrease appetite, increase metabolic rate and increase physical activity. As you accumulate more fat, you secrete more leptin. This causes more fat to be burned. But if you become leptin resistant, your brain doesn’t hear your fat telling it that it’s already full. Both inflammation and obesity cause leptin resistance. Leptin resistance is almost always present in obesity because it’s a precondition of significant fat gain. It’s impossible to gain more than a few pounds without being leptin-resistant.
Leptin resistance and inflammation set the stage for impaired fat and glucose metabolism, which in turn cause insulin resistance – the defining characteristic of metabolic syndrome and T2DM.
Diabesity is dangerous, so take care of yourself now!