Gut Bacteria

How Belly Fat Causes Inflammation and Promotes Autoimmune Diseases

by Mike Mutzel


People with too much body fat, either overweight or lean but metabolically obese (AKA skinny fat)  are more susceptible to infections and related complications, periodontal disease, and even autoimmunity. Common inflammatory diseases linked with excess body fat include rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), inflammatory bowel disease (IBD), multiple sclerosis (MS), type-1 diabetes (T1D), psoriasis and psoriatic arthritis (PsA), and auotimmune thyroid disease (i.e.Hashimoto thyroiditis). But why?

Obesity in autoimmune diseases: Not a passive bystander
Obesity in autoimmune diseases: Not a passive bystander. Autoimmunity Reviews 13 (2014) 981–1000

It turns out that belly fat, is sick. This deep, intra-abdominal or visceral adipose tissue (VAT) is very close to intestinal organs and is highly inflammatory. (In contrast, subcutaneous adipose tissue (SAT) on the upper arms, back, legs, and buttocks has little, if any, harmful immune or metabolic effects.)

Unlike subcutaneous fat of the upper arms, visceral fat tends to attract metabolically disruptive immune cells such as macrophages and lymphocytes. These immune cells release inflammatory messengers, or cytokines, that antagonize your metabolic machinery, disrupting your fat-loss efforts and creating a vicious cycle of more inflammation and fat accumulation. Unsurprisingly, an apple shape is associated with many of the metabolic and inflammatory diseases that occur with increased body fat percentage. This is why I call it “sick fat.”

Why is Belly Fat So Inflammatory

There are four main ways that fat increases inflammation:

  • Increased leptin release (which impacts Treg cells)
  • Increase adipose tissue hypoxia
  • Reduced adiponectin release

Lets discuss  in more depth.

Enlarged Fat Cells Become Devoid of Oxygen, Stimulating Inflammation

As fat cells enlarge when a person gains weight, progressing from lean to overweight to obese, oxygen availability to cells declines. This, in combination with other cellular stress messengers, triggers a key signaling molecule called hypoxia-inducible factor 1 alpha (HIF-1α). Increased HIF-1α is linked to changes in the inflammatory predisposition of immune cells, such as increased type 1 macrophage and the Th-17 type of T lymphocytes. This “immune signature” is linked to metabolic abnormalities, such as impaired fat burning and insulin resistance.

The combination of increased leptin and low oxygen levels in fat tissues that increase HIF-1α. That response, in combination with the surge of leptin, suppresses the immune cell guardians, the Treg cells that keep other T cells and inflammatory macrophages at bay.

By default, hypoxia is incongruent with oxygen-dependent fat burning, and so the only way immune cells can meet their increased energy demands in response to inflammation promoters like endotoxin, or HIF-1α from low oxygen, is to burn sugar as fuel.

Reduced Leptin Signaling Reduces Treg Cells Around Fat Tissue, Driving Inflammation

Yes. It’s complicated. Here’s another way to look at it: in their healthy state, working tissues, including immune cells, use oxygen to burn fat. For example, some immune cells (M2 macrophage, Th2, and Treg cells) rely heavily on fat for energy. Not so for the metabolically challenged, insulin-resistant, inflamed immune cells in fat tissue, the ones that are characteristic of obesity. These cells, which make up about 40 percent of fat tissue, shift out of fat-burning mode into sugar-burning mode.

Obesity in autoimmune diseases: Not a passive bystander. M. Versini et al. / Autoimmunity Reviews 13 (2014) 981–1000
Obesity in autoimmune diseases: Not a passive bystander. M. Versini et al. / Autoimmunity Reviews 13 (2014) 981–1000

Inflammatory triggers such as bacterial endotoxin favor immune cells that thrive on sugar burning, including the M1-type macrophage and Th1 and Th17 types of T helper cells. Unfortunately, these cells also induce inflammation, which is counterproductive to insulin sensitivity and fat burning.

In contrast, our steady-state anti-inflammatory cells, including the M2 macrophage and Treg cells, are great fat burners. Their existence is heavily dependent on proper levels of the mitochondrial regulatory factors discussed above, including AMPK.

Summary and Conclusion

Belly fat is highly inflammatory and is linked with many inflammatory diseases. Worse yet, the immune signature of inflammation (from increase fat tissue) creates an situation where sugar burning is attenuated, in favor of fat burning; further creating inflammation.

Whether fat loss is a goal, or reducing inflammation and recovering from autoimmune disease is your goal, targeting both the fat cells and immune system are key tactics to reclaim balance in your body.

In my book Belly Fat Effect: The Real Secret About How Your Diet, Intestinal Health, and Gut Bacteria Help You Burn Fat I discuss many novel strategies to help accomplish both of these goals. You can preview the book right here on 


Mutzel, M. (2014). Belly Fat Effect: The Real Secret About How Your Diet, Intestinal Health, and Gut Bacteria Help You Burn Fat. Wilsonville Media.


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