Fuctose makes you very Fat
High fructose corn syrups are the principle cause of the First World's obesity epidemic. Many scientists, medics and nutritionalists given a basic understanding of biochemistry have known this for years.
It's one thing though to know something and quite another to go up against the food industry whose 'counter-clout' or more explicitly, their ability to destroy you, rivals that of big pharma or, as in the past, the tobacco industry*.
After all isn't obesity caused by taking in too many calories, especially calories 'hidden' in liquid or pre-masticated, semi-digested food products in which lurk fats and sugars? It's simple, isn't it? And so accordingly foodstuffs are now labelled clearly with nutritional information listing fats, sugars and of course calories to help us controll our intake.
Usually fat in obesity debates gets the lion share of the blame on account of the energy density per gram that fats have. Then comes generic sugars as the new popular villain while more specific types of sugar; like fructose, lactose and oligi sacharrides usually escape scrutiny.
Finally there is a dawning awareness that all calories from whatever source are not equivalent. That is, maybe calories from sugars are not 'one to one 'equivalent to calories from proteins and fats. How can this be?
Whatever, the situation is multifactorial, complex and a full understanding requires biochemical knowledge of intermediary metabolism outside the scope of nutritionalists and medics in general.
So, given the above, how can we say fructose, a single sugar, abundant in fruits is alone as the chief driver of obesity?
The answer is simple.
Anyone with a basic knowledge of intracellular glycolysis and oxidative phosphorylation will tell you that fructose is handled differently to other simple sugars like glucose and galactose.
Glucose dominates the simple sugars being derived from starches, maltodextrins and other oligosacharrides as well as from 'sugar' sucrose and 'milk-sugar' lactose {sucrose = glucose+fructose, lactose = glucose+galactose}. Unsuprisingly glucose is carefully regulated both outside and inside the cell whether by the insulin system or enzymatic control. Fructose is not.
A paper published in the journal Obesity, elegantly and triumphantly spotted something simple and profound. They studied animals preparing for hibernation. Naturally animals that do hibernate need to maximise fat reserves for the winter sleep. In order to do this the calories you take in must exceed that calories you expend but what is the best way to prioritise fat storage in the autumnal feeding phase?
The animal is active during this phase, very active foraging, so it does not want to use a gramme of its fat reserves as energy. Fortunately at this time sugars but especially fructose in fruit is abundant. They found that fructose did two jobs, these were, a) putting on fat and b) conserving exsiting fat deposits.
The biochemical explanations were not in the scope of the paper but they are very clear from a metabolic control point of view. Fructose 'screams' unregulated through the pathway known as glycolysis. Glycolysis is used to break down glucose to provide the simple molecular 'food' for mitochondria which they then fully oxidise to generate energy and biosynthetic power.
The problem is that mitcondria cannot handle unlimited amounts of their molecular food known as 'acetyl' a simple two carbon atom molecule combined with hydrogen and oxygen. They can only process a limited amount and even this depends on the level of demand created by activity of the cell and the animal that it belongs to. In order to stop a catastrophic build up of acetyl it is turned into fat which can be safely ( from a biochemical perspective) stored in adipose tissue.
Clearly in a fructose rich environment one can easily visualise evey last gram of ingested fructose going straight to fat.
So, what of humans rather than hiberanting mammals? Well, due to our lifetsyles being so inactive many of the mitochondria especially in muscle will already be down-regulated, some will be nearly dormant. Now, add a fructose rich diet, eg high-fructose syrups in biscuits, cakes, candy and fruit-rich products like juices and yoghurts and the mitochondria will be 'maxed out' quite quickly.
Now, and here's the key, and the one made clear by the authors in Obesity: add a modest amount of any other foodstuff to the diet: lean meat, fish, bread, whatever and the calories are not going anywhere .. except as fat storage.
This means that with high fructose diets, the total calorie count means less than the composition of the diet. You can reduce your calorie intake substantially and yet get very much fatter ... how cruel but how obvious when you look around you.
1) The fructose survival hypothesis as a mechanism for unifying the various obesity hypotheses
Richard J. Johnson, Laura G. Sánchez-Lozada, Miguel A. Lanaspa
First published: 17 October 2023 https://doi.org/10.1002/oby.23920
*the vape nicotine comeback is pretty impressive so don't count themm out.
