Replace Fructose With Starch Can Improve Metabolic Health — Here’s Why


The science from fast food to soft drinks to fructose to starch to fruits — maybe it’s not so much about starches after all.
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What’s in Fast-food That Promote Weight Gain?

A 2014 study by the World Health Organization (WHO) investigated the relationship between fast food consumption and BMI in 25 high-income countries. “After adjustment for covariates, each 1-unit increase in annual fast food transactions per capita was associated with an increase of 0.033 BMI,” the study found. “Only the intake of soft drinks — not animal fat or total calories — mediated the observed association.”

This study means that soft drinks are an independent predictor of weight gain, regardless of the fast food. Soft drinks are responsible for the effects of fast food on weight gain, in other words.

But what about studies showing otherwise?

“The Literature is Polluted”

A 2013 systematic review by Maira Bes-Rastrollo, a professor of preventive medicine and public health at the University of Navarra, and colleagues looked at 17 systematic reviews that examine the link between soft drinks and weight gain. They found that,

  • 10 out of 12 systematic reviews without any conflict of interest concluded soft drinks as a possible risk factor for weight gain.
  • 5 out of 6 systematic reviews with financial support from food industries concluded otherwise.

Another 2016 study by the professor of medicine, Dean Schillinger and his team at the University of California, discovered the same. The title of their paper sums it up nicely, “Do Sugar-Sweetened Beverages Cause Obesity and Diabetes? Industry and the Manufacture of Scientific Controversy.” Systematically searching the literature about the effect of soft drinks on diabetes or obesity outcomes, they unraveled that,

  • 26 studies (8 clinical trials and 18 systematic reviews/meta-analyses) showed no relationship, of which 25 studies had financial support from food industries.
  • 34 studies (20 clinical trials and 14 systematic reviews/meta-analyses) showed soft drinks promote diabetes or obesity, of which only one study had financial support from food industries.

“The literature is polluted,” Emeritus Professor Robert Lustig at the University of California said at a 2020 conference in response to these studies. “It’s polluted on purpose because then they [the soft drink industry] can go back and say “see it’s inconclusive,” which is what they’ve been doing for the last 50 years.”
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What’s in Soft Drinks?

It’s carbonated water with sweetener, typically sugar. Sugar is sucrose. Sucrose is made of glucose and fructose in a 1:1 ratio. While glucose can be metabolized by cells throughout the body, fructose is primarily processed in the liver.

Liver fat is much more of a poison than visceral fat when it comes to insulin sensitivity and metabolic health. Excessive fructose becomes liver fat when glycogen stores are tanked — a phenomenon well replicated in rodent, primate, and human experiments. Adding fat or alcohol to a fructose-rich diet worsens liver fat accumulation and metabolic health, whereas omega 3 fatty acids can blunt fructose toxicity.

Importantly, glucose enhances the uptake of fructose. What’s in soft drinks again? Glucose-fructose units called sugar or sucrose.

Where’s the Fructose?

Fructose is naturally present in honey and fruits. In the modern Western diet, however, fructose is predominantly sourced from table sugar and high-fructose, especially in soft drinks, according to a 2018 research review in the prestigious Journal of Hepatology.

The same review also analyzed statistical data from different studies, showing a concomitant rise in table sugar intake and the prevalence of obesity and non-alcoholic fatty liver disease from 1988 to 2012 in the US.

Beyond the Liver, In the Gut

The liver mainly metabolizes fructose by the enzyme, fructokinase C. This enzyme is also present in the small intestines at substantial levels. But fructose metabolism in the small intestines is inflammatory as it loosens the tight junctions holding the intestinal barrier in place.

This is what happened when scientists at the University of Hohenheim gave mice fructose-containing drink. These mice had elevated levels of endotoxins in their bloodstream — a sign of leaked bacterial toxins from the gut. This metabolic endotoxemia did not occur in mice given glucose-containing drinking water. And it’s even intriguing that, in this study, mice that drank glucose consumed overall higher calories than mice that drank fructose.

A messed up gut messed up 12 other organs in the body, including the liver.

“Despite similar total energy, fat, protein, and carbohydrate intakes, patients with non-alcoholic fatty liver disease consumed significantly more fructose than controls,” a study found. These patients also had higher endotoxins in their blood that correlated with biomarkers of liver damage. For this reason, scientists believe that fructose induces fatty liver directly and indirectly via its interactions with the intestinal wall.
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The Case for Swapping Fructose for Starch

In a 2017 study, Professor Lustig and his team replaced the sugar in the obese children’s diet for starch. Starch is made up of linked glucose-glucose units and is present in carbohydrates like rice, wheat, pasta, or potatoes. The children’s daily consumption of fructose decreased from 12% to 4% of calories, but the researchers ensure that their calories remain the same. This is to ensure that the effects seen would not be a result of reduced caloric intake.

After only nine days of fructose restriction, liver fat decreased from 7.2% to 3.8%, visceral fat decreased from 123 to 110 cubic centimeter (cm3), and the liver fructose-fat conversion decreased from 68% to 26%. Insulin sensitivity measured by the oral glucose tolerance test improved as well. Importantly, their weight remained the same. In a separate analysis looking at a subgroup of these children, Professor Lustig also noted a decrease in blood pressure, triglycerides, and LDL cholesterol compared to baseline.

Maybe it’s not so much about the glucose in starches — rice, bread, pasta, potatoes, etc. — after all.

These children’s metabolic health improved from fructose (and not caloric) restriction. “They were making less fat in their liver, even though they’re getting just as many calories and more glucose,” Professor Lustig said. “We reversed their metabolic syndrome with no change in calories and no change in weight.”

Chronic overconsumption of fructose lowered metabolic rate and fat oxidation too, as shown by the 10-week fructose-sweetened soft drinks experiment in overweight/obese adults. This impaired metabolism is absent in those assigned with glucose-sweetened beverages. Another 10-week study replicated this finding: Fructose-sweetened, but not glucose-sweetened, drinks decreased insulin sensitivity while increasing visceral and liver fat.

It’s the fructose in table sugar and high-fructose corn syrup that deprives humans of metabolic health.

Notably, these kinds of calorie-controlled studies looking at glucose vs. fructose showed no differences in metabolic health if the experiment is only two to four weeks long (references a, b, and c).

Back to the title: Can swapping fructose for starch improve metabolic health? Yes, if the person is overweight or obese with a high intake of fructose. What about lean or healthy people? Yes, biochemically speaking. The liver would still convert excess fructose, with nowhere else to go, into fat.

The Fruit Argument

“While fruits contain fructose, they are less likely to induce metabolic syndrome due to the lower fructose content per fruit (compared to a soft drink) and also because they contain constituents (flavonols, epicatechin, ascorbate, and other antioxidants) that may combat the effects of fructose,” the 2018 review paper wrote.

But concentrated fruit juice or excessive amounts of fruit would still induce liver fat accumulation. Take nature, for example. Animals binge on fruits and honey to store fat as fuel during food shortages.

“Fructose metabolism is a primary nutrient used by many animals to gain fat mass,” a 2020 research review by researchers from the USA, Sweden, UK, Japan, and Korea wrote. “This has been shown to occur in long-distance migrating birds before their flights, in bears and other mammals preparing for hibernation, and also in certain types of fruit-eating fish such as the Pacu.”

This article was originally published on Medium with minor modifications.

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