Inflammation, Obesity, Immunity, and the Brain

Sometimes discovery involves a long and often painfully exacting process of connecting seemingly disparate bits of information. By 2014, researchers had begun to suspect that shedding extra fat somehow improves brain function.

There was evidence that losing weight through exercise and other non-invasive methods could help people think better, and a study of patients who had undergone bariatric surgery confirmed this. (Conversely, it appeared that putting on extra weight could harm the workings of the brain.)

Seventeen obese women were given cognitive function tests before surgery and then retested after, when they performed better, particularly when it came to executive function. This seemed meaningful because executive functions include organization and planning, and if there is one thing a post-bariatric surgery patient needs, it is the ability to keep their ducks in a row — to have a program and follow it, and not go off on impulsive binges that would stretch their newly restricted stomachs and undo all the good work.

Multiple factors

Along the way, it was discovered that the brains of the obese subjects metabolized sugars more quickly than the brains of normal-weight women. Separate research had revealed that obese people are about 35% more likely to develop Alzheimer’s Disease than their normal-weight fellow citizens.

New areas of inquiry opened up, like the possibility that body fat somehow increases proteins in the brain that touch off a cascade of events, making the person more vulnerable to Alzheimer’s. Fat cells were found to produce interleukin-1, which is known to cause severe inflammation, another condition that can impede the brain’s processes.

And another thing — visceral fat was associated with the probability of developing insulin resistance, about which journalist Alexandra Sifferlin wrote,

Insulin resistance has become linked to neurodegenerative diseases like Alzheimer’s because insulin resistance is associated with an increase in fatty acids, inflammation and oxidative stress. Insulin resistance is a metabolic disorder, that can be brought on by obesity.

Inflammation began to be viewed as potentially guilty of paving the way for various disorders, including “brain-related diseases, and even depression.” Body fat began to be viewed as potentially guilty of making all kinds of other things go haywire.

Less than a year ago, a scientific article bore the title “Adipose tissue inflammation in obesity: a metabolic or immune response?,” in which the question mark is the operative symbol. It said,

In addition to its roles in energy storage and as an endocrine organ, adipose tissue is increasingly recognised as an important immune organ. Obesity is now accepted as a low grade, chronic inflammatory disease that is linked to metabolic disorders, including type 2 diabetes and insulin resistance.

However, because of the complex combination of factors originating in the immune system and the endocrine system, it is still not clear exactly what goes on in the microenvironment known as adipose tissue.

Many substances

Adipose tissue, aka fat, generates at least 50 proteins, and some of them have been heavily incriminated in messing with metabolism and insulin sensitivity. Leptin was the first to be explored, and there is one called adiponectin, which “enhances insulin sensitivity by increasing fatty acid oxidation and reducing glucose production in the liver.”

One known as IL-6 “has pro-inflammatory and anti-inflammatory properties” and behaves in confusing ways. Adipose tissue secretes other pro-inflammatory and anti-inflammatory chemicals, and apparently it is vital that they be kept in balance.

But how? This report says,

At present, despite the efforts made to dissect the different cellular cross talk present within the adipose tissue, it is difficult to identify the initiating event(s) in the development of adipose tissue inflammation, though it appears likely to represent both a metabolic and an immune process.

This whole area of causation is multi-factorial to the point of nightmarish confusion, but scientists are unraveling the mysteries one by one.

Your responses and feedback are welcome!

Source: “This Is What Weight Loss Does To Your Brain,”, 08/27/14
Source: “Adipose tissue inflammation in obesity: a metabolic or immune response?,”, December 2017
Image source: mikebaird/Visualhunt

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About Dr. Robert A. Pretlow

Dr. Robert A. Pretlow is a pediatrician and childhood obesity specialist. He has been researching and spreading awareness on the childhood obesity epidemic in the US for more than a decade.
You can contact Dr. Pretlow at:


Dr. Pretlow’s invited presentation at the American Society of Animal Science 2020 Conference
What’s Causing Obesity in Companion Animals and What Can We Do About It

Dr. Pretlow’s invited presentation at the World Obesity Federation 2019 Conference:
Food/Eating Addiction and the Displacement Mechanism

Dr. Pretlow’s Multi-Center Clinical Trial Kick-off Speech 2018:
Obesity: Tackling the Root Cause

Dr. Pretlow’s 2017 Workshop on
Treatment of Obesity Using the Addiction Model

Dr. Pretlow’s invited presentation for
TEC and UNC 2016

Dr. Pretlow’s invited presentation at the 2015 Obesity Summit in London, UK.

Dr. Pretlow’s invited keynote at the 2014 European Childhood Obesity Group Congress in Salzburg, Austria.

Dr. Pretlow’s presentation at the 2013 European Congress on Obesity in Liverpool, UK.

Dr. Pretlow’s presentation at the 2011 International Conference on Childhood Obesity in Lisbon, Portugal.

Dr. Pretlow’s presentation at the 2010 Uniting Against Childhood Obesity Conference in Houston, TX.

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