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Fructose intake is a driver of obesity, just like in hibernating animals, study finds

by Kelsea Pieters, CU Anschutz Medical Campus

Obese photo

Researchers have identified a central conduit to obesity: fructose.


This study is a comprehensive review and synthesis of findings to date about fructose, putting this in the framework of a 'unifying theory' that encompasses both the existing evidence, and other theories.

The authors explain how the consumption of fructose affects metabolism in ways that not only 'drive' weight gain and obesity, but also lead to a wide range of mental symptoms, including lack of energy and motivation, that are typical of 'hibernation' - and for which specific mechanisms have recently been discovered.

Fructose is found naturally in fruits and sweet vegetables - and importantly, there is no evidence that fructose is likely to cause health problems when consumed via these foods.  However, its presence in ancestral, pre-industrial diets was therefore seasonal - following the main harvest-time - and also very low compared with typical modern, western-type diets.  

These kinds of diets - high in ultra-processed foods and drinks - provide fructose as an 'added' sugar, and in far higher quantities than our ancestors ever ate. 

Fructose makes up 50% of ordinary 'table sugar' (the other half is glucose), and a slightly higher proportion of 'high fructose corn syrup' (HFCS), which is used to sweeten numerous types of ultra-processed foods and drinks.

Abundant evidence now links high consumption of ultra-processed foods and drinks in general, and fructose in particular, with the so-called 'metabolic syndrome' which involves disturbances of both glucose and lipid metabolism.  This syndrome typically precedes the development of Type 2 diabetes, obesity, and other 'Non-Communicable Diseases' (NCDs), and also predicts risks for many mental health conditions. 

For details of the underlying research, see:

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01/08/23 - Medical Express

Researchers at the University of Colorado Anschutz Medical Campus have officially identified a central conduit to obesity: fructose.
While fructose's contribution to obesity is well-known, a study published today in Philosophical Transactions of the Royal Society B: Biological Sciences aggregates a large amount of work to make a full argument for how fructose drives obesity and diseases such as diabetes and fatty liver disease.
"This is an in-depth review on a hypothesis that puts nature at the center of weight gain, examining how fructose works differently than other nutrients by lowering active energy," says Richard Johnson, MD, professor at the University of Colorado School of Medicine and study lead author.

"We determine a recently discovered function of fructose in survival that stores fuel in case resources become scarce. This is known as the 'survival switch,'" he says.
Fructose is the source of sweetness in fruit, but is primarily consumed in Western society as table sugar and high fructose corn syrup, much different than the nutrition ingested by our ancestors ahead of lean winter months. Johnson and researchers posited that fructose works differently than other nutrients by lowering active energy, damaging mitochondria.
Study results show that fructose stimulates food intake and lowers resting energy metabolism, much like an animal preparing to hibernate. Further, results show that the administration of fructose can lead to weight gain, insulin resistance, elevated blood pressure and fatty liver among a host of other metabolic-related issues.
"This work puts together in one place the full argument for how a particular carbohydrate, fructose, might have a central role in driving obesity and diabetes," says Johnson.

"This is a very exciting, new hypothesis that unites other hypotheses to point to the specific role fructose plays in the onset of obesity. And we can trace it back to our ancestors, as well as learn from hibernating animals, exactly how fructose causes this 'switch' within us."