High fructose consumption increases the risk of fatty liver disease.

High fructose consumption increases the risk of fatty liver disease.

A new review shows how chronic excessive consumption of fructose, particularly from soda and ultra-processed foods, can quietly damage your liver. Diet and lifestyle changes remain the most effective tools for prevention. 

Study: Role of excessive fructose consumption on liver health. Image source: New Africa/Shutterstock.com

Fructose is a natural simple sugar found in many fruits and vegetables, in honey and especially as added sugar in processed foods. Excessive consumption of fructose is associated with non-alcoholic Fatty liver disease (NAFLD). A recent review in  Clinical Nutrition Open Science investigates the connection between this largely preventable disease and fructose. 

introduction

Fructose is a main ingredient in many high-calorie foods. It is used as a sweetener, particularly in the form of high fructose corn syrup (HFCS), a very tasty and inexpensive sweetener widely used in the food industry.

• HFCS enthält 55 % Fructose und 41 % Glukose.
• Es ersetzt Zuckerrüben- oder Traubenzucker in vielen Limonaden.

Chronic high consumption of sweeteners containing fructose has been linked to addiction-like effects in several experimental and clinical studies. HFCS has effects distinct from glucose alone and is associated with increased risks of fatty liver disease, insulin resistance, and obesity. The increasing use of HFCS coincides with the increasing incidence of NAFLD and metabolic syndrome.

The effects of fructose on metabolism can vary depending on gender and body mass. Some metabolic changes persist even when fructose intake is reduced. Mothers with high fructose consumption appear to pass on changes to their offspring, reprogramming their fructose metabolism and predisposing them to changes in fatty liver disease that may precede obesity or insulin resistance.

Unlike glucose, fructose is metabolized quickly and directly in the liver. Fructose metabolism largely bypasses insulin regulation, with many of its metabolic intermediates being processed in the liver, while some may enter the bloodstream. Large amounts of fructose can be metabolized by the liver, providing substrates for multiple metabolic pathways.

A significant amount of fructose is stored as energy or deposited as glycogen. Excess fructose is converted into fat, which is stored in the liver. This condition often leads to NAFLD and insulin resistance.

NAFLD and NASH

NAFLD is an umbrella term for a group of disorders characterized by excessive fat buildup in the liver without a history of excessive alcohol consumption. Fatty liver is the simplest and most common form, characterized by the accumulation of large, fat-rich vacuoles in liver cells.

Additional dietary fructose increases the risk of NAFLD as well as visceral obesity, hypertension, elevated triglycerides, and other liver diseases. Interestingly, fructose induces the new synthesis of fatty acids more strongly than glucose.

Rapid fructolysis also increases the release of fatty acids and very low-density lipoproteins (VLDL), leading to fat accumulation in skeletal muscle and the development of insulin resistance. Insulin resistance, which is part of metabolic syndrome, triggers, perpetuates and exacerbates fat-related changes in the liver.

In a significant proportion of patients, NAFLD progresses to nonalcoholic steatohepatitis (NASH), which is driven primarily by oxidative stress and mitochondrial dysfunction that occurs in response to free fatty acid toxicity: the so-called double-hit hypothesis.

In addition to fatty liver changes in the absence of alcohol exposure, NASH is characterized by periportal inflammatory infiltration and distention of liver cells. The affected liver cells are overloaded with triglycerides. Contributing factors include increased absorption of free fatty acids from the blood, improved new synthesis of triglycerides from fructose and other carbohydrates, and reduced fatty acid oxidation.

NASH is much more common in people with metabolic syndrome and is considered to be its hepatic manifestation. It can ultimately lead to serious liver damage.

Nutrition and NAFLD

Aside from a high-fructose diet, a high-fat diet activates the endocannabinoid axis, which alters fat metabolism toward obesity and insulin resistance. Type 1 cannabinoid receptors in the liver respond to activation by endocannabinoids by increasing insulin resistance and reducing beta-oxidation of fats.

A diet high in fructose, cholesterol and saturated fat exacerbates this Inflammation and metabolic damage.

Conversely, NAFLD can be stopped or even reversed by switching to a low-fructose and low-fat diet and moderate physical activity. Such measures have been shown to be effective in reducing liver inflammation and improving metabolic markers and liver health within just one month in some studies.

There are currently no specific drug treatments for NAFLD, making prevention and non-pharmacological treatments an urgent priority. A healthy diet with low fructose intake is one of the most important prevention strategies.

The Mediterranean diet is an excellent example of such a diet. Following the Mediterranean diet not only promotes cardiovascular and metabolic health and reduces the risk of cancer, but also reduces the risk of NAFLD. Therefore, several professional associations recommend this diet for patients with NAFLD/NASH.

The ketogenic (“keto”) diet reduces insulin secretion and inhibits fat synthesis while promoting fat oxidation. In addition, ketone bodies are created, which can reduce liver inflammation and fibrosis, suppress insulin resistance, and improve liver mitochondrial function.

An energy-restricted diet is another regimen that improves energy balance, promotes weight loss, and effectively reverses NAFLD compared to other diets. A dose-response relationship was found between the amount of energy restriction and the extent of weight loss and improvement in liver function. A 5% weight loss reduces liver fat, while a 7% reduction counteracts inflammation in the liver. Liver fibrosis improves with weight loss of more than 10%.

Conclusions

Excessive fructose consumption is a significant risk for the development and prognosis of NAFLD.

In general, a healthy diet and exercise pattern combined with lifestyle changes is the basis for the prevention and treatment of NAFLD.

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