A new study has found that the excessive consumption of fructose which is a sweetener common in the American diet, can lead to non-alcoholic fatty liver disease (NAFLD) which is comparably abundant in the U.S. However, contrary to previous thought, researchers are now reporting that fructose only adversely affects the liver after it has reached the intestines. Here the sugar disrupts the epithelial barrier which protects the internal organs from bacterial toxins in the gut.
NAFLD is the most common cause of chronic liver disease throughout the world and it can progress to more serious conditions. The new findings point to an approach that could prevent damage to the liver in the first place.
Consumption of fructose in the U.S. has been skyrocketing since the 1970s with the introduction of high fructose corn syrup (HFCS). This is a cheaper sugar substitute that is commonly and broadly used in packaged and processed foods such as cereals, baked goods and soft drinks.
Multiple studies in humans and animals have linked increased HFCS consumption to some of the nation’s numerous inflammatory conditions such as heart disease, cancer and diabetes, and also the nation’s obesity epidemic. Currently the U.S. FDA regulates it similar to other sweeteners such as honey or sucrose and advises only moderate intake.
The new study defines a specific role and risk for HFCS in the development of fatty liver disease. Interestingly, the ability of fructose which is plentiful in dates and dried figs to induce fatty liver was known to the ancient Egyptians who fed geese and ducks dried fruit to make their version of foie gras.
With the advent of metabolic analysis and modern biochemistry, it has become obvious that fructose is two to three times more potent than glucose in increasing liver fat which is a condition that triggers NAFLD. The increased consumption of soft drinks that contain HFCS is linked to the explosive increase in NAFLD incidences.
Fructose is broken down in the digestive tract by an enzyme known as fructokinase which is produced both by the gut and the liver. By using mouse models, researchers discovered that excessive fructose metabolism in intestinal cells reduces the production of proteins that maintain the gut barrier. This is a layer of tightly packed epithelial cells that are covered with mucus to prevent bacteria and microbial products such as endotoxins from leaking out of the intestines and into the blood.
Through deteriorating the barrier and increasing its permeability, excessive fructose consumption can lead to a chronic inflammatory condition called endotoxemia which has been shown in both experimental animals and pediatric NAFLD patients.
The researchers in the current study found that leaked endotoxins that reach the liver provoke increased production of inflammatory cytokines and stimulated the conversion of fructose and glucose into fatty acid deposits. It is very clear to the team that fructose does its harm in the intestine and if intestinal barrier deterioration is prevented, the fructose does little harm to the liver.
The team has noted that feeding mice with high amounts of fructose and fat will result in particularly severe adverse health effects. This is a condition that mimics the 95th percentile of relative fructose intake by American adolescents who get close to 21.5 percent of their daily calories from fructose. And this is often in combination with calorie dense foods such as french fries and hamburgers.
The team did find that when fructose intake was reduced below a certain threshold, no adverse effects were noted in mice. This suggests that only excessive and long-term consumption of fructose represents a health risk. Moderate fructose intake by normal consumption of fruits appears to be well tolerated.
Unfortunately, there are many processed foods that contain HFCS and most people are unable to estimate how much fructose they are actually consuming. Increased awareness and education are the best solutions to this problem, however for those people who have progressed to the severe form of NAFLD known as nonalcoholic steatohepatitis, these findings offer some ray of hope of a future therapy based on the restoration of gut barrier.
To view the original scientific study click below