Major Study Claims to Identify Root Cause of Obesity
Fructose, a new paper proposes, is the pernicious little demon driving so many human metabolisms 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 a decision to lose weight may not come down to a choice between ditching either carbs or fats, but a case of responsibly reducing both together.
Unfortunately, having significant quantities of the carbohydrate fructose in your diet won’t make that so easy.
“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. Balanced by the vitamins and fiber therein, your daily apple, banana, and orange isn’t so much an issue. The body can also make small amounts of fructose from carbohydrates such as glucose, and salty food.
Added to sweeteners such as table sugar and high fructose corn syrup in high quantities, concentrations of this particular sugar can quickly pile up in our diet, often without our realizing.
Johnson and his colleagues undertook 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), which provides energy for your body’s cellular processes.
When ATP falls to a low enough level, it’s a signal to your body that you need more fuel. This makes you hungry, so you eat.
Diagram showing how fructose survival theory ties other obesity theories together. (Johnson et al., Obesity, 2023)
This is what the researchers call the fructose survival hypothesis, and it 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.”
This low power mode activates even if there are fuel reserves at hand. Even when there is plenty of available energy in the form of stored fat, fructose blocks the body from tapping into any of that storage.
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.
See more here sciencealert.com
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Tom
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Now you know why it is in so many foods. Eat more, weigh more.
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Richard
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My 62 year study on myself has found if I eat more more I put on weight . Moreover also founding eating less didn’t make me fatter – that astounded me after years of hearing obese people tell me it’s not about how much you eat .
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VOWG
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It is amazing is it not. I have maintained the same weight, give or take a pound or two for over 50 years. Still the same at 80 plus.
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Richard Greene
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Of course you failed to mention that “same weight” is 495 pounds. Keep up the good work.
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Richard Greene
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People also get less exercise with so much time spent n front of phone, computer and TV screens. Jumping to conclusions in a comment section is not real exercise.
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Richard
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As I sit here writing this on my phone I am also peddling on my under the desk pedal machine .
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Howdy
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“Jumping to conclusions in a comment section is not real exercise.”
Very scientific. That’s the second jibe you made about people who comment on PSI today. Why are you here if it’s so bad?
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Richard Greene
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I’m here because some articles are good AND I RECOMMEND THEM ON MY BLOG’S DAILY LIST OF GOOD ARTICLES FROM CONSERVATIVE WEBSITES.
I thought the 495 pound joke was funny.
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Cal Aylmer
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Ba ha ha ha
People will tie them selves into knots trying to excuse their inability to stop filling their pie holes. Lookit NOT ONE FATTY came out of Auswits!.
Proof positive.
If its a “glandular problem” as the fatties have clung to for decades how come we don’t see one single fat body in the concentration camps. Nope sorry people. Eat more than you burn off in a day and a little extra gets piled on for later.
FAT PEOPLE HAVE FAT PETS AND FAT KIDS, NORMAL PEOPLE HAVE NORMAL PETS AND NORMAL KIDS, SKINNY PEOPLE HAVE SKINNY PETS AND SKINNY KIDS. Explain that one. I reckon its the PEOPLE deciding what a portion size for themselves and their pets looks like. Have you seen the trollies of the fatties in the grocery store piled high with cardboard boxes of fake food and chips and fizzy drinks.?
In my day they taught NUTRITION in primary school. and we were allowed on the monkey bars.
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Howdy
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“NOT ONE FATTY came out of Auswits”
You’re an animal Cal.
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M
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Does anyone have access to a PDF of the research paper? The link in the article reveals that the paper is behind a paywall, but any commenter who has institutional access (schools, universities, workplace, etc) could obtain a copy freely. Cheers.
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