How Inflammation Causes Obesity and Diabetes

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There is mounting evidence linking inflammation to obesity and Type 2 diabetes. Today you’ll understand why inflammation may be the most important mechanism contributing to obesity and diabetes.

The connection between inflammation and obesity/diabetes is still a hot topic in the scientific world, even though it’s nothing new. The association between these conditions has been known for decades, if not longer.

A Diabetes Cure Discovered Over 100 Years Ago

More than 100 years ago high doses of salicylates, a class of anti-inflammatory compounds which includes aspirin, were used to treat Type 2 diabetes. In 1876, a physician named Ebstein found that sodium salicylate could eradicate the symptoms of diabetes. However, this treatment is no longer used because of serious side effects caused by high doses of salicylates.

“Aspirin can cause several forms of liver injury:  in high doses, aspirin can cause moderate to marked serum aminotransferase elevations occasionally with jaundice or signs of liver dysfunction, and in lower doses in susceptible children with a febrile illness aspirin can lead to Reye syndrome.”

Questions that Need to be Answered

1. Do obesity and diabetes cause inflammation, or is the opposite true?

2. How does the body initiate an inflammation response to obesity/diabetes, and under what conditions does this response occur?

3. Does obesity itself cause inflammation, or is inflammation caused by secondary effects due to obesity such as high blood glucose levels or high triglyceride (blood fats) levels?

This article will present current information and research concerning those questions and more.

How Inflammation Causes Obesity and Diabetes

There is compelling evidence that inflammation directly causes obesity and diabetes.

1. Inflammation has been shown to precede the development of obesity/diabetes. Elevated levels of inflammatory cytokines predict future weight gain. Injecting inflammatory cytokines into healthy, normal weight mice cause insulin resistance.

“Insulin resistance in case of obesity is commonly accompanied by low-grade systemic inflammation and adipose tissue inflammation.”

Research Abstract: Inflammation, cytokines and insulin resistance.

The supposition that inflammation precedes obesity/diabetes is supported by the observation that humans with other chronic inflammatory conditions are at higher risk of developing Type 2 diabetes.

For example, about one-third of chronic Hepatitis C patients develop Type 2 diabetes, and people with rheumatoid arthritis are also at higher risk.

2. Inflammation begins in the fat cells. Fat cells are the first to be affected by the development of obesity. As fat mass expands, inflammation increases.

Two possible mechanisms:

A. Dysfunction of cellular mitochondria caused by the added stress obesity places on cellular function.

B. Oxidative stress caused by excessive amounts of glucose available to fat cells, hyperglycemia. When this occurs, high levels of reactive oxygen species (ROS – free radicals) are produced that start an inflammation cycle within the cell.

3. Inflammation of the fat tissue (adipose) causes insulin resistance, which is the primary feature of Type 2 diabetes.

A small protein called a cytokine, released during the inflammatory response, has been repeatedly shown to cause insulin resistance. Several other proteins involved with inflammation have been implicated with causing or contributing to insulin resistance.

4. Inflammation of the brain (specifically the hypothalamus) causes leptin resistance, which often precedes and accompanies insulin resistance and Type 2 diabetes.

Leptin is a hormone that regulates appetite and metabolism. It does this through its effect on the hypothalamus. When the hypothalamus becomes resistant to leptin, glucose and fat metabolism are impaired and weight gain and insulin resistance result.

How Obesity and Diabetes Cause Inflammation

Fat has always been considered an inert tissue. It didn’t do much other than store excess energy. But that view has changed.

Important: It’s known, however, that fat tissue is a metabolically active endocrine organ that secretes hormones and inflammatory cytokines.

The metabolic activity of fat is the key to understanding its role in obesity/diabetes.

How could obesity cause inflammation?

There are two basic theories.

#1: Obesity-induced inflammation is a protective mechanism that prevents the body from becoming less fit; or from another perspective, less agile. Fat storage is an anabolic process, which means it builds up the organs and tissues.

Inflammation, on the other hand, is a catabolic process. Catabolism breaks down organs and tissues. The line of reasoning is the activation of catabolism via inflammation is the body’s attempt to maintain weight within optimal limits.

Evidence that experimentally induced local inflammation in fat tissue improves insulin resistance and causes weight loss supports this theory.

#2: Obesity-induced inflammation is a malfunction that was never selected against in human evolution.

Obesity and its related secondary disorders have been extremely rare throughout human history. These conditions became prevalent and epidemic within the past 40 years.

From Harvard University:

“In 1990, obese adults made up less than 15 percent of the population in most U.S. states. By 2010, 36 states had obesity rates of 25 percent or higher, and 12 of those had obesity rates of 30 percent or higher.”

Source: An Epidemic of Obesity: U.S. Obesity Trends

And this is limited data but still interesting; 100 years of US obesity:

The evolution of BMI values of US adults: 1882-1986

It’s possible that the stresses of obesity are sufficiently similar to the stresses of an infection that the body reacts to obesity in the same way it would to an infection: via inflammation.

Supporting this theory is evidence that the same intracellular, inflammatory stress pathways are activated in both obesity and infection.

Whichever theory is correct, it’s clear that obesity/diabetes cause inflammation.

1. Insulin and leptin resistance impair glucose metabolism.

2. When fat cells become insensitive to insulin, they can’t store any more glucose and hyperglycemia results.

3. Excess blood sugar causes glycation, a process in whick a sugar molecule binds to a protein or a fat cell and forms advanced glycation endproducts (AGEs).

AGEs are inflammatory and are associated with Type 2 diabetes.

Click on image to zoom.

4. Obesity also contributes to inflammation by affecting particular genes involved with the inflammatory response. These genes control the expression of white blood cells called macrophages that play a key role in inflammation.

5. As the concentration of macrophages in the fat tissue increases, the release of inflammation by-products also increases.

Important: This means that the more fat tissue you have, the more inflammation it will produce.

Wrap-up

The evidence suggests that inflammation is both the cause and the result of obesity/diabetes.

Once obesity and/or insulin resistance have been established, each can further stimulate the production of inflammation, thus inducing a vicious cycle of inflammation and obesity/diabetes.

Important: The key to preventing and treating obesity/diabetes is reducing inflammation.

Focusing only on regulating blood sugar and fat hormones without addressing other potential causes of inflammation amounts to fighting half the battle.

What are these “other causes” of inflammation?

Overall, the 21st century style of living.

Specifically…

  1. Dietary triggers (wheat products, refined sugars, processed cooking oils from various seed sources, and other triggers.)
  2. Stress
  3. Poor sleep
  4. Gut bacterial imbalance
  5. Environmental toxins

These all cause inflammation on their own. But taken together, they’re more powerful and more harmful.

For now, the takeaway is inflammation is probably the single most important mechanism driving the obesity/diabetes epidemic. And you do have positive control over the various external, environmental factors contributing to inflammation.