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French Fry Hypothesis Results Suggests New Anti-Obesity Tactic

Tim Boyer's picture
French Fry and Obesity

We have known for years that salt in our diet is the bugaboo of good health. However, researchers have recently discovered that testing a French fry hypothesis by varying the salt content in the diets of mice on a high fat diet suggests a new anti-obesity tactic that may be the answer to treating obesity in man.


Let’s face it - we love salt and we love fat. Put the two together and we have the best of two worlds of flavor. Unfortunately, however, each separately contributes to weight gain. But did you know that the two together do not necessarily add up to even more weight gain?! In a new study published in the journal Scientific Reports, researchers discovered that when mice were fed a high salt and high fat diet that they gained less weight than those on a low salt, high fat diet.

In a study based on what the researchers referred to as their “French fry hypothesis” it stood to reason that adding high salt to a high-fat diet would naturally result in increased weight gain. To test this hypothesis, groups of mice were separately fed a high fat diet with varying amounts of salt ranging from low (0.25%) to high (4.0%).

However, rather than find that the mice on a high fat and highest salt diet gained the most weight, it turned out that the mice on the fat diet with the lowest salt content were the ones to actually gain the most weight―up to 3 times as much weight over a 16-week long test period.

According to a news release from the University of Iowa:

"We found out that our 'French fry' hypothesis was perfectly wrong," says Justin Grobe, PhD, assistant professor of pharmacology at the UI Carver College of Medicine and co-senior author of the study. "The findings also suggest that public health efforts to continue lowering sodium intake may have unexpected and unintended consequences."

However, the results don’t mean that you should be reaching for the salt shaker just yet. Looking a little deeper into the potential causes of this salt-factored weight gain dichotomy, the researchers determined that their results were linked to salt’s effects on calorie absorption efficiency.

"This suppression of weight gain with increased sodium was due entirely to a reduced efficiency of the digestive tract to extract calories from the food that was consumed," explains Grobe.

"Our study shows that not all calories are created equal," added Michael Lutter, MD, PhD, co-senior study author and UI assistant professor of psychiatry. "Our findings, in conjunction with other studies, are showing that there is a wide range of dietary efficiency, or absorption of calories, in the populations, and that may contribute to resistance or sensitivity to weight gain."

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As it turns out, salt affects the activity of an enzyme called renin―a component in the hormonal renin-angiotensin system (RAS) that mediates the control of digestive efficiency by dietary sodium. And, since the level of salt in a high fat diet was found to affect weight gain in mice, this means that it may be possible to control weight gain by interfering with a person’s digestive efficiency in their digestive tract.

In fact, the authors point out that reducing digestive efficiency has been proven by one weight loss drug “Orlistat” a.k.a. “Alli” that is used for aiding weight loss. Hence, controlling the renin-angiotensin system could lead to the development of new anti-obesity treatments.

“…we hypothesize that further investigations into mechanisms (such as the RAS and its AT2 receptor) that control digestive efficiency may lead to the development of more efficacious anti-obesity therapeutics,” conclude the authors of the study.

For additional articles that include info about reducing digestive efficiency through Orlistat for weight loss, click-on the three provided below:

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Scientific Reports June 2015 “Dietary Sodium Suppresses Digestive Efficiency via the Renin-Angiotensin System

University of Iowa news release― “High salt prevents weight gain in mice on a high-fat diet