Fructose, a new paper has found, is the pernicious little demon driving the human metabolism towards obesity. Although it’s not the biggest source of caloric intake, it does trigger the urge to eat fattier foods, at higher quantities, resulting in overindulgence in food.
A major analysis, led by medical doctor Richard Johnson of the University of Colorado Anschutz Medical Campus, suggests that the best way to lose weight is by reducing intake of not sugars or carbs alone, but both together.
“Although practically all hypotheses recognize the importance of reducing ultraprocessed and ‘junk’ foods, it remains unclear whether the focus should be on reducing sugar intake, or high glycemic carbohydrates, or fats, or polyunsaturated fats or simply increasing protein intake,” the researchers write in their paper.
“Here, we review the various dietary hypotheses for obesity. We propose that all of the various hypotheses are largely correct, and that although they outwardly seem incompatible, that they can all be unified based on another hypothesis known as the fructose survival hypothesis.”
Fructose is a type of sugar that can naturally be found in fruit, where it is balanced by the vitamins and fiber therein. But it’s also in sweeteners such as table sugar and high fructose corn syrup, in much higher quantities. The body can also make fructose from carbohydrates such as glucose, and salty food.
Johnson and his colleagues made an exhaustive study of all the known contributors to obesity, and found that the metabolism of fructose in the body causes a drop in a compound called adenosine triphosphate (ATP). ATP provides energy for your body’s cellular processes; when ATP levels fall to a low enough level, it’s a signal to your body that you need more fuel. This makes you hungry, so you eat.
This is what the researchers call the fructose survival hypothesis, and ties together different theories of what causes obesity, even those that seem wildly incompatible, like fat intake versus carbohydrate intake.
“Essentially, these theories, which put a litany of metabolic and dietary drivers at the center of the obesity epidemic, are all pieces of a puzzle unified by one last piece: fructose,” says Johnson. “Fructose is what triggers our metabolism to go into low power mode and lose our control of appetite, but fatty foods become the major source of calories that drive weight gain.”
But it’s a false low power mode. Fructose only mimics a state of low energy by reducing ATP in the body’s cells, even when there is plenty of available energy in the form of stored fat. Fructose basically blocks the body from tapping into that stored energy.
In some contexts, that’s a good thing. Bears preparing for hibernation can keep their fat reserves intact by chowing down on fruit. But consumption of sugary foods and drinks in humans, the researchers say, is the way towards unhealthy excess.
“This evolutionary-based mechanism is used to assist animals in the storage of fat when food is still available before an expected food shortage,” the researchers write. “Although meant to aid survival in the short term, with chronic over-engagement this pathway shifts from being beneficial to driving many of today’s modern diseases.”
More research is required to determine exactly how this works, since most of the research into how fructose works is based on animals. However, the findings represent an important step in resolving this escalating health crisis.
The research has been published in Obesity.
