Inflammation underlies most diseases.
The purpose of inflammation is to help the body heal and protect against further damage. However, chronic inflammation is harmful and involved in the development of many lifestyle diseases, such as heart disease and diabetes.
Recently, researchers tested the effects of sugar on inflammatory markers. Here is a detailed summary of their findings.
Regularly eating a lot of sugar has adverse health effects.
It’s linked with increased calorie intake and obesity, as well as low-grade, chronic inflammation.
However, not all sugar is the same. Several types of sugar are found in your diet, the most common of which are:
- Glucose: This is the most important sugar in your body and used by most cells for fuel. It also makes up your blood sugar. Glucose is stored in your muscles and liver as glycogen.
- Fructose: Also known as fruit sugar, fructose is found in many plants and often connected to glucose in the form of sucrose. Since your body’s cells (except for sperm cells) cannot use fructose, it is changed into glucose by the liver.
- Sucrose: Commonly known as table sugar, sucrose is composed of one glucose molecule and one fructose molecule connected together. In the gut, digestive enzymes split sucrose into glucose and fructose.
These three sugars are found in numerous syrups and sugar-based sweeteners, such as high-fructose corn syrup, which usually contains about 55% fructose and 42% glucose.
Additionally, animal experiments suggest that eating high amounts of fructose may weaken the gut wall (intestinal barrier) and allow bacterial toxins to “leak” into the blood, causing systemic inflammation (3, 4).
This study compared the effects of different types of sugar – glucose, fructose and high-fructose corn syrup – on markers of inflammation.
No differential effect of beverages sweetened with fructose, high-fructose corn syrup, or glucose on systemic or adipose tissue inﬂammation in normal-weight to obese adults: a randomized controlled trial.
This randomized controlled crossover trial examined the effects of different types of sugar — fructose and glucose — on markers of inflammation.
Obesity and fat gain, especially in the belly area, is associated with inflammation. To isolate the effects of sugar, the researchers tested participants’ short-term (8-day) intake of sugar before they started to gain significant amounts of fat.
The study recruited 24 lean to obese men and women aged 18–65. None of them had fructose malabsorption.
The participants were assigned to one of three 8-day study periods in a random order. During each study period, they were asked to consume sugar-sweetened beverages, which differed by the type of sugar used:
- Glucose: Aspartame was added to match the sweetness of the fructose beverage.
- High-fructose corn syrup: 55% fructose, 41% glucose. Aspartame was added to match the sweetness of the fructose beverage.
Each of the beverages accounted for 25% of the participants’ estimated calorie requirements per day. Otherwise, the participants followed a standardized diet provided by the research kitchen.
Since the study had a crossover design, the participants consumed all three beverages during different study periods, separated by a 20-day washout period.
At the start and end of each period, the researchers measured the following:
- Inflammatory markers: C-reactive protein (CRP), interleukin-6 (IL-6) and adiponectin.
- Fat tissue inflammation: 14 participants agreed to undergo a belly skin fat biopsy to measure fat tissue inflammation.
- Intestinal permeability: The researchers measured markers of intestinal permeability (zonulin and lipopolysaccharide-binding protein (LBP)) and also did the lactulose-mannitol test.
Bottom Line: This was a randomized controlled trial testing the effects of excessive, short-term sugar intake on inflammatory markers.
Finding 1: Sugar Did Not Increase Inflammatory Markers
Participants’ levels of inflammatory markers remained unchanged during the study.
Specifically, drinking high amounts of beverages sweetened with glucose, fructose or high-fructose corn syrup (HFCS) did not affect the circulating levels of C-reactive protein (CRP), interleukin-6 (IL-6) or adiponectin, as shown in the charts below:
Similarly, excessive sugar intake did not significantly affect inflammation in fat tissue.
Supporting these findings, one previous study in obese and overweight people showed that consuming fructose-sweetened beverages for 10 weeks did not affect CRP or IL-6 (6).
Another study found that high fructose and glucose consumption for 4 weeks did not affect CRP. Visceral belly fat did not change and PAI-1 and MCP-1 remained unchanged (5).
Taken together, these findings suggest that fructose itself does not promote inflammation. However, it might promote inflammation through its effects on belly fat.
Bottom Line: The study showed that short-term (8-day), excessive intakes of fructose or glucose (dissolved in water) did not affect the inflammatory markers CRP and IL-6.
Finding 2: Sugar Intake Did Not Affect Markers of Intestinal Permeability
Intestinal permeability refers to the ability of the intestinal barrier to control the movement of water-soluble substances from the intestines into the blood.
When intestinal permeability is higher than normal, such as when the bowels are damaged or weakened, it is sometimes called a “leaky gut.”
Several tests can be used to assess intestinal permeability. The most common test is the lactulose-mannitol test, but the current study also measured circulating levels of zonulin and lipopolysaccharide-binding protein (LBP) (10).
The researchers discovered that eating excessive amounts of fructose, glucose or high-fructose corn syrup did not affect markers of intestinal permeability. These findings are presented in the charts below.
Previous animal experiments indicate that excessive fructose intake may cause inflammation in the gut wall, increasing its permeability.
However, the present study suggests that 8-day, excessive intakes of fructose don’t similarly affect humans.
Bottom Line: Excessive consumption of sugar (fructose or glucose) for 8 days did not affect markers of intestinal permeability.
This study had no apparent methodological limitations. However, the findings should be interpreted cautiously.
The testing periods were short. Therefore, the study doesn’t rule out that excessive sugar intake may increase inflammation and intestinal permeability when eaten for longer periods.
Summary and Real-Life Application
In short, this study showed that eating excessive amounts of sugar — fructose and/or glucose — for 8 days did not affect markers of low-grade, chronic inflammation in lean and obese adults.
It is likely that some of the adverse effects of high fructose consumption develop slowly over a long period, perhaps in association with increased liver fat and visceral fat.
However, there is no doubt that eating less sugar has immediate health benefits, especially in obese individuals who regularly eat high amounts of sugar.