Fructose, inflammation and cortisol as a cause of visceral fat
What it found
The authors propose that eating too much fructose causes inflammation in cells that break it down quickly, and that this inflammation raises cortisol inside cells.
That chain of events, they suggest, leads to fat being stored around organs rather than under the skin.
What they found
Inflammation in cells
The authors propose that eating too much fructose leads to inflammation in all cells that break it down quickly. This is a proposed mechanism, not a measured result.
Cortisol in fat cells
When fructose is broken down in fat cells under the skin, the authors suggest the inflammation that follows raises cortisol inside those cells. This higher cortisol is described as the body's attempt to calm the inflammation.
Fat moving to organs
The authors propose that the rise in cortisol inside fat cells under the skin makes more fatty acids leave those cells. Those fatty acids then provide more material for fat storage in visceral fat tissue.
Fatty liver
The authors suggest that fructose-induced inflammation in the liver raises cortisol inside liver cells through an increase in 11-B hydroxysteroid dehydrogenase type 1. They say this leads to more fat storage in the liver, known as fatty liver.
Thin outside, fat inside
The authors describe the whole chain, from fructose to inflammation to cortisol, as causing what they call "thin on the outside, fat on the inside" (TOFI).
Fructose in the brain
The authors propose that fructose in the brain, either taken up from the blood or made there from glucose, triggers more cortisol release. They say this leads to the liver making glucose and to overall insulin resistance, and further body fattening.
What the authors conclude
“This review paper will discuss in detail the hypothesis that fructose-induced inflammation and cortisol activation causes visceral adiposity.”
Also in their conclusions
- They propose a new mechanism for body fattening, in particular visceral adiposity, involving the overconsumption of fructose.
- They state that the fructose-induced inflammatory cortisol response causes "thin on the outside, fat on the inside" (TOFI).
- The authors say this review paper will discuss in detail the hypothesis that fructose-induced inflammation and cortisol activation causes visceral adiposity.
How it was done
The usual idea that obesity comes from eating more calories than you burn does not explain why some people store fat in and around their organs. Another common idea, that added sugars and refined carbohydrates cause insulin resistance and high insulin, also does not explain visceral fat.
What it can’t tell you
- We summarised it from the abstract only.
- This is a proposed mechanism, not a set of experiments in people or animals.
- It cannot show that fructose actually causes visceral fat in people.
- The steps in the chain, from fructose to inflammation to cortisol to fat storage, have not been confirmed by the studies described here.
Who paid
- Authors work at
- Saint Luke's Mid America Heart Institute, United States; MGM Medical College, India; Kempegowda Institute of Medical Sciences, India
The paper
- Title
- Fructose-induced inflammation and increased cortisol: A new mechanism for how sugar induces visceral adiposity
- Type
- ReviewThe authors read earlier studies and describe what they found. It isn’t a new study.
- Summarised from
- Abstract only
- Cite
- DiNicolantonio JJ, Mehta V, Onkaramurthy N, O'Keefe JH (2018). Fructose-induced inflammation and increased cortisol: A new mechanism for how sugar induces visceral adiposity. Progress in cardiovascular diseases. doi:10.1016/j.pcad.2017.12.001PubMed 29225114DOI
Summary written 26 Sep 2026. Check it against the paper before it changes what you eat. How we summarise papers · Report an error