What is Diabesity, and how to reverse it

Important Points:

  • Diabesity
  • Type 2 diabetes
  • Insulin resistance
  • Obesity
  • Sedentary lifestyle

What is Diabesity, and how to reverse it

If you are like most people you are probably thinking that I have confused diabetes for diabesity, or you are probably wondering whether I intended to say obesity. You are not so far away from the truth as diabesity is a modern disease that links obesity with type 2 diabetes. Diabesity should be a concern for people with normal blood sugars who may be accustomed to unhealthy eating and lifestyle patterns. It is unfortunate that much is not mentioned about diabesity which can predispose you to severe obesity, diabetes, and other fatal chronic conditions.

What Is Diabesity?

Diabesity is a sequence of events that starts with optimal blood sugar balance, to progressive insulin resistance, to being overweight, then becoming obese, and finally to full-blown Type-2 Diabetes. It comes in a spectrum that includes elevated blood sugar, elevated blood pressure, high cholesterol, and other health complications. These problems stem from diet, lifestyle, and environmental toxins interacting with our unique genetic susceptibilities. A study published in NCBI in 2013 concluded that “(diabesity) makes a strong call for utilizing indigenous, low-cost means of enhancing healthy dietary and physical activity habits.” Diabesity can also be described as the coexistence of obesity and type 2 diabetes.

What Are The Triggers For Diabesity?

Diabesity occurs following the development of insulin resistance and obesity. When your diet is full of empty calories: quickly absorbed sugars, liquid calories (soda, juice, sports drinks), and refined carbohydrates, you are likely to develop a resistance to insulin. Insulin (produced by beta cells in the pancreas) is the hormone that is responsible for grabbing glucose out of the bloodstream and storing it in cells. This ensures that blood sugar levels remain stable in the blood. When the body starts ignoring the signal sent out by insulin we call this insulin resistance. Beta cells will keep releasing more and more insulin to try to remedy the situation, so a high insulin level is one of the first signs. Unfortunately, the higher your insulin levels are, the worse your insulin resistance becomes. High insulin levels will also cause a spike in appetite which leads to overeating. Very soon you develop weight gain around the belly, more inflammation, oxidative stress, and other effects such as high blood pressure, high cholesterol, low HDL, atherosclerosis, and increased risk of cancer, Alzheimer’s, and depression.

It is important to note here that the root cause of the problem is insulin resistance and not elevated blood sugar. Fortunately, insulin resistance can be reversed since it is strongly linked to poor diet and an unhealthy lifestyle.

Most people can save themselves from diabesity by eliminating the factors that are upending the balance of their biology and replacing them with what’s needed to help the body re-balance itself.

Diabesity and Genetics

Many people believe that insulin resistance and diabesity are genetic conditions that cannot be extraneously controlled. True enough, our genetic predisposition plays a role in the way we choose what to eat and how to live. It also plays a role in the development of insulin resistance. However, insulin resistance and diabesity are greatly influenced by diet and lifestyle, so controlling these factors can greatly minimize your chances of developing the conditions.

How To Reverse Diabesity

Before reversing diabesity, there are a few things you can do to keep safe. They include:

1.   Know the signs of insulin resistance.

One of the first tell-tale signs of insulin resistance is uncontrollable weight gain. You might also experience increased blood pressure and skin discoloration (acanthosis nigricans) on rare occasions. Unfortunately, insulin resistance may go unnoticed for years. Hence, you may be better off having some tests done.

2.  Get the right tests done

You should get tested if you have a positive family history of type 2 diabetes and are affected by a poor diet as well as a sedentary lifestyle. An insulin response test is the best test to tease out the condition.

If you have already been diagnosed with diabesity, here are three things you can do to start your reversal journey.

Make healthy diet choices

This may involve the input of your physician, nutritionist/ dietician, and yourself to come up with the right meal plan. A healthy diet will start with the elimination of sugary and processed foods. Opt for wholesome grains, fresh vegetables and fruits, nuts, white meat, and unsaturated fats instead. You can read more about this type of diet here. (hyperlink to foods that improve insulin sensitivity).

Get adequate rest

Stress is a major contributor to insulin resistance and blood sugar imbalance. Stress also contributes to making unhealthy food choices and overeating. You need to make a conscious effort to de-stress frequently by:

  • Sleeping for at least 7 hours daily
  • Practicing relaxation techniques such as yoga
  • Taking breaks in between work like every two hours
  • Taking sabbaticals and vacationing periodically

Quit a sedentary lifestyle

Modern jobs involve sitting at an office desk and hitting the keypad hours on end. In a world where work is compensated by the hour, it can be difficult to make time for exercise. However, when you consider the negative long-term effects of a sedentary lifestyle you will be forced to reconsider the value of the extra money. What is the point if it’s going to cost your health in the long run? Quitting a sedentary lifestyle involves making deliberate choices about exercise and fitness. This may mean walking at least 30 minutes every day or engaging in more vigorous aerobic exercise 4-6 times a week.


1.   Science Daily (2012): Genetic variant is linked to obesity and insulin resistance. Retrieved from

2.   NCBI (2011): Is fast food addictive? Retrieved from

3.   NCBI (2013): Diabesity. Retrieved from



Understanding the role metabolic inflammation plays in obesity and diabesity

Important Points:

  • Inflammation
  • Obesity
  • Diabesity
  • Insulin resistance
  • Adipose tissue

Understanding the role metabolic inflammation plays in obesity and diabesity

Obesity is a disease that has plagued the modern day man in recent time. Access to highly processed foods and decrease in physical activity are key contributors to this ailment. Researchers are hard at work looking into what other underlying factors lead to obesity, especially given its relationship with the onset of Type 2 Diabetes, Cardiovascular diseases, and liver disease. We will take an in-depth look at metabolic inflammation and its role in the onset of obesity. Let’s dive in.

1. What is Obesity?

Obesity is a state in which there is an over-accumulation of subcutaneous and/or abdominal fat (adipose tissue) characterized by a low grade chronic state of inflammation in which the level of pro inflammatory cytokines are increased.  This adipose tissue is no longer considered inert and mainly devoted to storing energy; it is emerging as an active tissue in the regulation of physiological and pathological processes including immunity and inflammation.

  Weight (Pounds) x 703       OR         Weight (Kilograms) 

Height (Inches) x Height (Inches)      Height (Meters) x Height (Meters)  

Obesity is diagnosed when your body mass index (BMI) is 30 or higher. To determine your body mass index, use one of these formulas:

BMI =  

BMI Weight status
Below 18.5 Underweight
18.5-24.9 Normal
25.0-29.9 Overweight
30.0 and higher Obesity

For most people, BMI provides a reasonable estimate of body fat. Because BMI doesn’t directly measure body fat, some people such as muscular athletes may have a BMI in the obesity category even though they don’t have excess body fat.

2. What is Diabesity?

‘Diabesity’ is the term for diabetes occurring in the context of obesity. This form of obesity-dependent diabetes has emerged as a major public health problem in recent times. Though it is basically explained by insulin resistance and pancreatic beta cell dysfunction, new patterns have evolved to explain these modifications in the context of the modern rates of obesity and diabetes.

3. Is Obesity an Inflammatory Condition?

The connection between obesity and inflammation has been in debate in the recent past. Unbeknownst to many, the link between these conditions was made decades ago. Over a century ago, high doses of a class of anti-inflammatory compounds including aspirin (salicylates) were used to treat Type 2 diabetes. In some cases, the symptoms of diabetes totally disappeared. Unfortunately, this treatment was discontinued due to the serious side effects caused by the high doses of salicylates.

We will now look at the questions of our topic today in-depth; does obesity cause inflammation, or is inflammation caused by something secondary to obesity such as high blood sugar or triglycerides levels? How about diabesity? Does diabesity cause inflammation, or does inflammation cause diabesity? How and why does the body initiate an inflammatory response to diabesity? Let us tackle each item separately.

4. How Does Inflammation Cause Diabesity?

Listed are some lines of evidence that show inflammation directly causes obesity and diabesity.

  • The development of diabesity has been shown to follow inflammation. Raised levels of inflammatory cytokines predict impending weight gain. In a study, infusion of inflammatory cytokines into healthy, normal weight mice caused insulin resistance. This concept is also illustrated by the fact that people with other chronic inflammatory conditions are at higher risk of developing Type2 Diabetes; for example, about one-third of chronic Hepatitis C patients develop Type 2 diabetes, and those with rheumatoid arthritis are also at higher risk.
  • In obesity, inflammation has been noted to start in the fat cells themselves. As fat mass expands, inflammation increases. One explanation may be that dysfunction of the mitochondria (the “power plant” of our cells) caused by obesity puts increased stress on cellular function. Another mechanism may be oxidative stress. As more glucose is delivered to the fat cells, they produce an excess of reactive oxygen species (ROS) which in turn starts an inflammatory cascade within the cell.
  • Inflammation of the fat tissue causes insulin resistance, which is the primary feature of Type 2 diabetes. TNF-α, a cytokine (small protein) released during the inflammatory response and several other proteins involved with inflammation, such as MCP-1 and C-Reactive protein have been repeatedly shown to cause insulin resistance.
  • 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 this through its effect on the hypothalamus. When the hypothalamus becomes resistant to leptin, glucose and fat metabolisms are impaired and weight gain and insulin resistance result.
  • When there is inflammation of the gut, there arises leptin and insulin resistance. This may occur via an increase in lipopolysaccharide (LPS), an endotoxin produced by Gram-negative bacteria in the gut. LPS has been shown to cause inflammation, insulin resistance in the liver, and weight gain.

5. How  does Diabesity Cause Inflammation?

In the past, fat was considered an inactive tissue with no biological action. It wasn’t considered for much other than storing energy. It has now emerged that fat tissue is a metabolically active endocrine organ that secretes hormones and inflammatory cytokines such as IL-6 and TNF-α. This metabolic activity of fat is the key to understanding its role in diabesity.

6. Why would obesity cause inflammation?

The first theory is that obesity-induced inflammation is a protective mechanism that prevents the body from losing mobility or fitness. Fat storage is an anabolic process, which means it builds up the organs and tissues. Inflammation, on the other hand, is a catabolic process which breaks down organs and tissues. It’s possible that the activation of catabolism via inflammation is the body’s attempt to keep weight within acceptable bounds. Evidence that experimentally induced local inflammation in fat tissue improves insulin resistance and causes weight loss supports this theory.

The second theory is that, obesity-induced inflammation is simply a malfunction that was never selected against in human evolution. Obesity and its related disorders have been extremely rare throughout human history, and have only become common in the past 40 years. The surplus of modern, processed foods that accompanies diabesity is also a relatively new phenomenon. It’s possible that the stresses of obesity are similar enough 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.

7. Tackling Inflammation in the control of diabesity

We can therefore conclude that inflammation is both the cause and the result of diabesity. Once obesity and/or insulin resistance have been established, each can further stimulate the production of inflammatory cytokines, forming a vicious cycle of inflammation and diabesity.  

Reduction of inflammation is a major key in preventing and treating diabesity. Focusing exclusively on regulating blood sugar and fat hormones without addressing other potential causes of inflammation is bound to produce inferior results.



Diabesity and Inflammation: A Case of Chicken and Egg

Important Points:

  • Diabesity
  • Diabetes
  • Obesity
  • Inflammation
  • Anti-inflammatory

Diabesity and Inflammation: A Case of Chicken and Egg

In a previous article, I introduced the term “diabesity”, the description of Type 2 diabetes when it occurs in the context of obesity. Insulin resistance is defined by an inability of the body to respond to insulin and use up glucose in the blood. When insulin resistance sets in and glucose builds up in the blood, pancreatic beta cells produce excess insulin in an effort to bring down that glucose level. Diabesity is triggered by the onset of insulin resistance.

Because diabesity is diabetes in the context of obesity, we have to recognize that inflammation caused by obesity also plays a role in the onset of diabetes. Here, we will discuss what role inflammation plays and why it might be the most important mechanism fueling the diabesity epidemic.

Why are anti-inflammatory drugs not the mainstay of diabetes type 2 treatment?

Before delving into the connection of the diabesity-inflammation pendulum, I decided to throw in a teaser.  This quote is taken from an article published in JCI in 2006 titled “Inflammation and Insulin Resistance.”

“Clues to the involvement of inflammation in diabetes date back to more than a century ago when high doses of sodium salicylate (5.0–7.5 g/d) were first demonstrated to diminish glycosuria in diabetic patients having type 2 diabetes. In 1876 Ebstein concluded that sodium salicylate could make the symptoms of diabetes mellitus totally disappear.”

Why then are anti-inflammatory agents not the mainstay of diabetes type 2 treatment? This is indeed a controversial topic. It is believed that sodium salicylate was dropped because of the serious side effects it causes when given in high doses.

Let’s move on to the pendulous relationship between diabesity and inflammation.

How does Inflammation Cause Diabesity?

There are several lines of evidence linking inflammation with obesity and diabetes; here are a few:

1.   Inflammatory markers are elevated prior to the diabesity

Elevated levels of inflammatory cytokines could indicate future weight gain and obesity . A lab study also showed that an infusion of inflammatory cytokines into healthy mice causes insulin resistance.

This idea is also supported by the fact that people with other chronic inflammatory conditions are more likely to develop diabesity and type 2 diabetes.

2.  Inflammation causes insulin resistance

Inflammation of the fat tissue causes insulin resistance, the primary cause of diabesity. A small protein known as TNF-α which is released during inflammation has been shown to cause insulin resistance, and other inflammatory proteins such as MCP-1 and C-Reactive protein have also been linked to insulin resistance.

3.  Inflammation in the brain causes leptin resistance

Inflammatory signaling in the hypothalamus has been linked to leptin resistance in both animals and humans. Leptin is a hormone produced in fat cells that sends signals to the hypothalamus in order to regulate hunger and energy. It is sometimes called the starvation hormone and sometimes the obesity hormone. Leptin resistance happens when your body is no longer responsive to leptin, causing your brain to be fooled into believing that you are starving need to keep eating more and more food. Eventually, this leads to diabesity.

How Does Diabesity Cause Inflammation?

For a long time, it was believed that fat is an inert tissue with no biological activity, however, it is now known that fat is a metabolically active endocrine organ that produces hormones and inflammatory molecules. The feature of fat is the key to understanding its role in diabesity and inflammation.

1.   Diabesity induces inflammation as a protective mechanism.

Diabesity causes the buildup of fat around the waist. Fat storage builds up in anabolic processes while inflammation breaks down in catabolic processes. The body may activate catabolism through inflammation so as to keep weight within acceptable limits. Experimentally induced inflammation in fat tissue has been shown to initiate weight loss and improve insulin resistance.

2.  Diabesity related stresses could cause inflammation

Obesity has been associated with chronic low-level inflammation. it is hypothesized that the stresses of diabesity are similar to the stresses caused by an infection. As a result, the body responds in a similar way by triggering inflammation.

Obesity has also been linked to the release of inflammatory compounds such as TNF-α, setting up a proportional connection between the amount of fat tissue you have and the amount of inflammation your body experiences.

The Chicken Versus the Egg

It is clear that there is a direct relationship between diabesity and inflammation, but it is very difficult to determine which comes first. Inflammation is both a major cause of diabesity and occurs as a result of diabesity.  On the other hand, the occurrence of diabesity can further stimulate the production of inflammatory cytokines forming a vicious cycle of inflammation and diabesity.

We believe the best approach towards the treatment or prevention of diabesity has to begin with addressing the underlying inflammation, and it should also involve treating inflammation once diabesity has occurred. Current modern clinical approach is focused on regulating blood sugar without addressing inflammation.  Unfortunately, such an approach is bound to produce inferior results.


1.   ADA: Inflammation-Sensitive Plasma Proteins Are Associated With Future Weight Gain.  Retrieved from

2.   NCBI (1993): Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance. Retrieved from

3.   NCBI (2012): Obesity is associated with hypothalamic injury in rodents and humans. Retrieved from

4.   JCI (2005): Inflammation, stress, and diabetes. Retrieved from