New research proposes fructose as the key driver of obesity, unifying various dietary theories. The “fructose survival hypothesis” suggests that fructose consumption depletes active energy and hinders appetite control, thereby contributing to an energy imbalance that promotes weight gain. This new perspective could guide more effective obesity prevention and management approaches.
Recent research led by CU Anschutz researcher Richard Johnson, MD, unifies a number of hypotheses behind the dietary cause of obesity that once seemed incompatible.
For a long time, nutrition specialists have understood that Western eating patterns, which are high in fats and sugars, might be a contributing factor to the obesity epidemic. However, there’s been ongoing contention about what drives the issue most significantly—is it the consumption of excess calories in general, the overconsumption of specific macronutrients like fats or carbohydrates?
In response to this uncertainty, various factions have advocated for different dietary approaches, with some suggesting a cutback on sugar, others advising a decrease in carbohydrate consumption, and still others proposing that the main focus should be on limiting the intake of foods high in fat.
Unifying Dietary Theories of Obesity
A paper recently published in the journal Obesity suggests these theories are not incompatible with each other, and that they can all be brought together in one unified pathway that centers around one true driver: fructose.
According to Richard Johnson, MD, University of Colorado Anschutz Medical Campus researcher, and his colleagues, the primary problem in obesity is fructose, which is present in table sugar and high fructose corn syrup. Fructose can also be made in the body from carbohydrates (particularly glucose). When fructose is metabolized, it lowers the active energy in the body (known as ATP, or adenosine triphosphate) which causes hunger and food intake.
The Fructose Survival Hypothesis
What Johnson calls the “fructose survival hypothesis” brings together most of the dietary hypotheses of obesity, including the two that have been most incompatible with each other– the energy balance theory, which proposes too much food (and primarily fat) drives obesity, and the carbohydrate-insulin model, which puts carbohydrates at the center of weight gain.
“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.”
To unify these theories in particular, Johnson says we can look to hibernating animals as an example. When we’re hungry and low on active energy, we go into survival mode. Animals know to forage for food when energy levels begin to fall; why bears eat fruit to prepare for winter. Fruits are high-fructose foods, and fructose significantly stifles active energy. Fat acts as stored energy, but eating high-fructose foods blocks the replacement of active energy from fat storage, keeping active energy low like a bear preparing for a long winter’s nap.
“This theory views obesity as a low-energy state,” says Johnson. “Identifying fructose as the conduit that redirects active energy replacement to fat storage shows that fructose is what drives energy imbalance, which unites theories.”
While more work is needed to fully validate this unifying hypothesis, this is a hopeful first step in potentially identifying more targeted preventions for obesity and related metabolic imbalance management.
Reference: “The fructose survival hypothesis as a mechanism for unifying the various obesity hypotheses” by Richard J. Johnson, Laura G. Sánchez-Lozada and Miguel A. Lanaspa, 17 October 2023, Obesity.
DOI: 10.1002/oby.23920
“There are too many theories on obesity. Let’s unite them all into one theory of obesity!”
Result: One additional obesity theory.
So…I can eat as much fat and carbs and sugar as I can, so long as I cut out fruit and added fructose? Great theory.
I don’t think you understood this article at all, the basic point is to eliminate any sort of processed sugar entirely. Yes you can eat as much high quality fat, not too much from meat or saturatws, that you want, and even some processed carbs, but what you fail to graps is that INDUSTRIAL food is basically too toxic to eat, what they don’t talk about here is how hyper-procesed food alters your gut biome too, stop being a smartass troll please
The article didn’t mention “processed” or “industrial” or “biome” anything. It did mention “According to Richard Johnson, MD, University of Colorado Anschutz Medical Campus researcher, and his colleagues, the primary problem in obesity is fructose, which is present in table sugar and high fructose corn syrup…Fructose is what triggers our metabolism to go into low power mode and lose our control of appetite”. So, fructose, that’s very specific. Their new ‘unified theory’ is that fructose increases hunger, makes the body store fat, and lowers energy use, creating obesity. You seem to disagree with that.
I avoid processed food, enjoying Pollan’s aphorism of only shopping around the periphery of the grocery store. It doesn’t seem to cause weight loss, but it’s definitely for health. I agree with you, but the article wasn’t about that at all.
Sucrose (table sugar) is composed of glucose and fructose. Eating as many carbs and fats as you can, also will obviously result in obesity, unless you exercise enough to use the calories. Try cutting out the fructose and sugar and eat as much as you need, not feel hungry. I suspect that eating salty snacks will also increase intake of carbs and calorie-rich drinks, even if you are not hungry.
Not to discourage Dr. Johnson or any other obesity researchers but, coincidental to my own mysterious, serious incident of chronic fatigue, generalized aches, pains and muscle weakness, serious mood swings and rapid weight gain in 1964 at age twenty, repeated and turned chronic at age thirty-seven with one major difference in early 1981, the culprits in the current global obesity pandemic are undiagnosed nearly subclinical non-IgE-mediated food allergy reactions (Dr. Arthur F. Coca, by 1935) aggravated (or not) with officially approved food poisoning (added cultured “free” MSG, minimally). The one big difference for me between 1964 and 1981 was the US FDA approval of the expanded use of allergy aggravating MSG as an alleged “flavor enhancer” in 1980, with the US obesity/diabetes epidemic presenting by 1990 (CDC/NCHS data).
As best as I’ve been able to determine as a lone lay investigator of forty-two years and counting, ineligible from the start for any of now trillions of medical research grant dollars, chronic inflammation caused by the very, very mild allergy reactions stimulates the release of xanthine oxidase which breaks down into uric acid and free radicals, causing mitochondria to switch from glycolysis (glucose-to-energy) to glycogenesis (glucose-to-fat). Individual allergen identification, partial avoidance of then identified allergens and added MSG and targeted nutritional supplementation may be sufficient to switch the mitochondria back to glycolysis. I’ve personally begun experimenting with recommended high doses of vitamin B9 (methylfolate) and B12 (to avoid pernicious anemia) with encouraging early results.
Viral infection?
Thanks but no, Paul, nearly subclinical non-IgE-mediated allergy reactions to proteins, lab tested and verified through at-home dietary experiments. Check out “The Pulse Test” by Dr. Coca, available free online in PDF format.
Like Bormated Vegitable Oil (BVO), the FDA should ban High Fructose Corn Surrip (HFCS) from all food NOW!
Bottom-line: If it tastes sweet, you should probably avoid it.