In this article, I’d like to present a unified model of diabesity. I think it’s helpful to have a “birds-eye view” of how diabesity begins and progresses. It gives us a context for the articles that will follow, each of which will examine specific elements of the model in much more detail.
Two caveats before we dive in. First, remember that all models are imperfect. They’re useful tools, but as the saying goes, a map is never the same as the territory itself.
Second, there is still much about the model I’m going to present that isn’t thoroughly understood. We’re on the bleeding edge here. The science is evolving rapidly, with new articles being published every day. What I’m presenting here is based on my interpretation of the information that is currently available. There are some parts of the model I’m more certain about than others, and I’ll point that out when applicable.
Okay, now that we have that out of the way, take a look at the following diagram. If you click on it a larger version will open in a new window. You might want to print this out or keep it open as we go, because I’ll be referring to it throughout the article.
That’s quite a mouthful, so let’s take a closer look at what each part of that statement means.
The innate immune system is the part of the immune system that 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.
Inflammation is the primary response of the innate immune system. In a healthy person, inflammation is temporary and the body eventually returns to homeostasis (“internal balance”). In the case of autoimmunity, however, the body mounts a response against its own cells and tissues and becomes stuck in a continuous loop of chronic inflammation.
Recent research suggests that diabesity is characterized by chronic, low-grade inflammation and a continuous stimulation of the innate immune system. The inflammatory state that accompanies diabesity is not associated with infection or other traditional signs of autoimmunity, and seems to have its own unique features.
Studies clearly show that the incidence of diabesity accompanies its adoption around the world. The features of this lifestyle that have been implicated include:
- Dietary toxins (primarily refined wheat, fructose and industrial seed oils);
- 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
Genetics also play a role in diabesity. 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. But genetics likely do explain why some individuals and populations are more likely to develop diabesity when exposed to a modern, western lifestyle.
Environmental factors (together with or independent of genetics) cause both inflammation and obesity, which are both strongly associated with type 2 diabetes (T2DM). But while obesity predisposes people to the metabolic changes characteristic of T2DM, it is not necessarily a feature of diabetes. Evidence is now clear that not all obese people have metabolic dysfunction, and that in some cases, obesity may even protect against metabolic and cardiovascular disease. In this sense obesity may be the body’s attempt to protect against the damage done by a modern lifestyle. (If you’re confused by this, don’t worry – we’ll cover it in more detail later.)
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On the other hand, inflammation nearly always accompanies both obesity and diabetes and is independently capable of causing it without overweight – as evidenced by the presence of T2DM in Asian populations that are relatively lean. This explains why thin people can have all of the metabolic problems commonly associated with obesity, including full-fledged T2DM. And in fact these cases of T2DM may be the most severe, because they lack whatever protective adaptation obesity may confer.
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.
Fat exists in the body in three primary forms: free fatty acids (FFAs, a.k.a. “non-esterified” fatty acids), triglycerides and phospholipids. Triglycerides and phospholipids are the storage forms of fat. FFAs can be transported in the blood without any carriers.
In healthy people, FFAs are burned in the mitochondria soon after release (lipolysis) from storage forms of fat (triglycerides and phospholipids). But in the diabese, inflammation, leptin resistance and oxidative damage impair the mitochondria’s ability to burn fats. The excess FFAs then “spill over” into non-fat tissue like the liver, pancreas and skeletal muscles. FFAs damage these metabolically active tissues because they don’t belong there. This is called lipotoxicity. Lipotoxicity has been shown in several studies to cause insulin resistance and increase the risk of T2DM.
Both inflammation and obesity cause leptin resistance. Leptin 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. 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.
Beta-cell destruction, which leads to the decline in insulin production seen in some cases of T2DM, can be caused by several mechanisms. These include genetics, inflammation, autoimmunity (i.e. Type 1.5 or Latent Autoimmune Diabetes in Adults [LADA]), and impaired fat metabolism (lipotoxicity) and glucose metabolism.
And here we arrive at our final destination: full-fledged type 2 diabetes. It is an autoimmune, inflammatory disorder triggered by modern lifestyle, influenced by genetics, and characterized by impaired glucose and fat metabolism and fat hormone resistance. The purpose of this article was to give you a broad overview of all of the elements of the model. In the articles that follow, we’ll look at each of them in much more depth.
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