Can Fatty Liver Disease Affect Your Bowels? Gut-Liver Connection Explained

Heather Campbell
 min read

Can fatty liver disease affect your bowels?

Can Fatty Liver Disease Affect Your Bowels? Gut-Liver Connection ExplainedFatty liver diseases are diseases characterized by an overload of fat in the liver cells called hepatocytes.

As a general rule, being overweight or drinking excessively can lead to liver disease and an imbalance in our gut microbiota. The liver is the first line of defense, and the onset and progression of steatotic liver disease is dependent, among others, on our intestinal microbiota’s composition.

Referred to by specialists as “steatosis” or “steatotic liver disease,” these disorders correspond to the accumulation of triglycerides (the storage form of fatty acids) in the hepatocytes (liver tissue cells).

Read on to learn how fatty liver disease affects your bowels.

Can fatty liver disease affect your bowels? Introduction

The causes of fatty liver diseases are multiple and primarily dominated by two conditions: overweight and excessive alcoholic drinking.

Currently, steatotic liver diseases are the most common liver diseases globally.

This article will uncover our liver’s role in our body and its relationship with our intestinal microbiota and how fatty liver disease affects your bowels.

The basics of the liver

Essential to our body, the liver is known for its role in digestion but also has other indispensable functions.

The liver is part of the digestive system and is one of the largest organs in the body. Find it by putting your hand on the right side of the abdomen, under the last rib.

The liver is our personal chemical complex

The functions of the liver are multiple and vital. It allows us to eliminate all our chemical waste, including medications, in bile or in our urine and is the only organ capable of eliminating cholesterol.

It manufactures multiple substances essential to our survival, such as blood proteins like albumin, necessary for blood coagulation.

The liver also allows us to store and restore our body’s energy. It stores food sugars in the form of glycogen in the hepatocytes (liver tissue cells) and returns them in the form of usable glucose for our muscles.

When glycogen stocks are depleted, the factory will start to manufacture glycogen from amino acids provided by proteins.

Fats are stored in the liver in the form of triglycerides which release their highly energetic fatty acids to meet the energy needs.

By being adapted to multiple functions, the liver is a critical organ in our energy regulation.

The liver is in contact with the blood coming from the digestive tract

The liver receives blood through two blood vessels. In fact, one-third of the blood that passes through it comes from the hepatic artery, which comes from the aorta and provides the oxygen needs of the channels carrying bile.

Two-thirds of the blood that irrigates the liver is brought by the portal vein, which drains all the venous blood, still highly oxygenated, from the digestive tract.

This blood supply allows the liver to fulfill its synthesis and storage missions by transforming all the nutrients that have been absorbed by the digestive tract.

The liver can also be the site of serious diseases

There are multiple liver diseases with various causes that can be genetic, infectious, toxic, or autoimmune cancerous.

Many of these diseases develop through a liver inflammation called “hepatitis” and can be due to various reasons (e.g., infection, a toxic substance, too much alcohol, etc.).

When inflammation is chronic, it will generate fibrous scars that disorganize the complex structure of the liver.

This disrupts the passage of blood through the liver, resulting in an increase in blood pressure in the portal vein upstream of the obstacle.

Cirrhosis may develop, which is characterized by a dilaceration of the liver by fibrous scars in rings isolating small nodules of hepatic cells. The liver then becomes lumpy and hard.

The pressure of the portal blood increases considerably, resulting in the formation of varicose veins similar to those that develop on some people’s legs.

In the case of portal hypertension, varicose veins develop all along the digestive tract (particularly around the esophagus and stomach), where they are likely to rupture, inducing serious digestive hemorrhages.

At the stage of cirrhosis, another complication can threaten the patients, namely, the insufficiency of the liver functions, called hepatic insufficiency. This is related to the incapacity of the sick liver to face the body’s needs.

The combination of portal vein hyperpressure and liver failure will expose patients to severe complications, such as:

  • swelling of the legs and belly that fill with fluid (ascites),
  • jaundice, or
  • brain and psychiatric disorders that can result in a coma.

Metabolic liver disease (steatosis)

Steatosis is very common in overweight and metabolic syndrome and is referred to as “non-alcoholic steatosis” or “metabolic steatosis” in non-drinkers.

The liver is the first line of defense

We need to look to the gut microbiota to understand why the steatotic liver becomes inflammatory.

The endotoxins will cross the intestinal wall and reach the liver via the portal vein blood mixed with chylomicrons (which are microscopic droplets of fat absorbed by the intestine or by bacterial translocation).

The liver is well-armed to defend itself and can eliminate endotoxins by excreting them in the bile after neutralizing them with cholesterol derivatives.

But the presence of endotoxins in the liver is dangerous because, before being neutralized, bacterial endotoxins can activate specific receptors of the brutal innate immunity at any time.

Obeying the activation of these receptors, the forces of immunity will trigger an inflammation, thus provoking collateral damage to the liver, which can become very harmful by perpetuating itself.

The liver is at risk when steatosis is complicated by inflammation

Pure steatosis does not, by itself, cause significant liver dysfunction.

In humans with excessive caloric intake, steatosis shows the severity of metabolic disturbances and a high risk of cardiovascular and cancerous complications.

In one out of three ill people, steatosis becomes inflammatory. In this case, it is called “non-alcoholic steatohepatitis.”

The appearance of inflammation in the liver shows that over time, the liver can deteriorate to the stage of metabolic cirrhosis. This affects 20% of patients with steatosis after about ten years of evolution.

The most severe stage of chronic liver disease is cirrhosis and sometimes a liver transplant is the only cure.

In the United States, metabolic cirrhosis has become the first indication for liver transplantation.

Therefore, early detection and treatment of patients with non-alcoholic steatosis are essential to prevent progression to cirrhosis.

Gut microbiota in non-alcoholic steatosis of the liver

The onset and progression of steatotic liver disease are dependent on:

  • what we eat,
  • how foods are transformed by our body by genetic heritage
  • the composition of our intestinal microbiota.

Microbial overgrowth in the small intestine is prevalent in steatotic liver disease

Usually, the small intestine microbiota in patients with steatosis is the site of excessive growth of bacteria, some of which secrete substances toxic to the intestinal wall.

The resulting alterations cause translocation, which plays a significant role in the aggravation of liver damage.

In addition to the inflammation it generates, translocation also induces fatty acid and triglyceride synthesis by the liver, thereby increasing steatosis.

Studies on rodents have shown that injections of endotoxins can cause weight gain and steatotic liver disease.

Abnormalities in the gut microbiota may be associated with the severity of liver damage

Research has been conducted on mice fed a high-fat diet, showing that they gained weight.

In addition, some will also develop metabolic complications such as insulin resistance and diabetes or steatotic liver disease. However, other mice gained weight without developing metabolic complications.

If we transplant the intestinal flora of these mice to germ-free mice, we notice:

  • After receiving the intestinal flora of mice that developed metabolic complications and steatotic liver disease, mice will develop the same complications on a high-fat diet.
  • But in contrast, mice that received the intestinal flora of those mice will not develop metabolic complications.

This experiment thus shows the essential role of the intestinal microbiota in metabolic complications and steatotic liver disease related to weight gain.

The microbiota abnormalities linked to the complications of overweight are a decrease in bacteria that protect against inflammation and an increase in bacteria such as lactobacilli, some of which produce dietary fibers and substances that are toxic to the liver through fermentation.

Intestinal dysbiosis associated with severe metabolic damage to the liver can also be characterized by a depletion of bacteria involved in transforming primary bile acids into secondary bile acids and whose concentration decreases.

The impact of this alteration is important, as these bile acids control the growth of bacteria in the small intestine and contribute to the maintenance of the impermeability of the intestinal barrier.

However, the decreased activation by bile acids of receptors located in the nuclei of cells has two serious consequences:

  • It reduces the protection against steatosis and inflammation of the liver that these receptors are responsible for.
  • And it decreases the synthesis of bile acids by the liver, aggravating the deficit in secondary bile acids.

When the microbiota becomes a distiller

The intestinal microbiota will produce small amounts of alcohol detected in the blood. Moreover, these quantities will increase in case of significant consumption of sugar.

The study of the bacteria that increase in the small intestine of patients with steatosis and steatohepatitis showed the presence of bacteria capable of making homemade but toxic alcohol.

Alcohol is a factor that aggravates the evolution of steatosis. Daily consumption of alcohol increases the risk of cirrhosis threefold in patients with metabolic steatosis.

As a result, the liver transforms alcohol into acetaldehyde which seems to be the cause of the increased risk of cancer through its toxic action on the DNA of our cells.

Diet and metabolic steatohepatitis

Dietary measures that can improve steatotic liver disease are the same as those for treating metabolic syndrome and obesity further showing how fatty liver disease affects your bowels.

Consuming Omega-3, a weapon against steatosis

Several studies have investigated the impact of dietary supplementation with long-chain omega-3 fatty acids on metabolic steatopathy in adults and children with obesity and metabolic syndrome.

Most often, omega-3s were in the form of fish or seal oil.

The meta-analysis of these studies showed that omega-3 intake improved metabolic syndrome and liver function.

Indeed, this intake reduces steatosis, but unfortunately, it does not seem to significantly impact inflammatory liver lesions.

A Mediterranean-type diet is preferred

One study compared the Mediterranean diet to the low-fat diet in improving liver fat overload and metabolic abnormalities.

The study showed that the Mediterranean diet was more effective than a low-fat diet in reducing steatosis and improving metabolic abnormalities associated with high cardiovascular disease risk.

  • The Mediterranean diet is based on fresh, seasonal products, fruits, vegetables, legumes, and grains excluding all processed products.
  • It is rich in good fats with the use of olive oil, and has little animal protein.
  • The consumption of fish and eggs is favored, and dairy products are mainly from sheep and goats.

Pro and prebiotics in the treatment of metabolic steatosis of the liver

Common probiotics (Lactobacillus, Bifidobacterium, and Streptococci) and butyrate-producing bacteria have shown interesting results in the treatment of metabolic steatopathies.

Studies have shown that probiotic treatment can:

  • improve blood markers of inflammation,
  • decrease insulin resistance, and
  • reduce blood levels of transaminases, the elevation of which is a sign of liver damage.

However, this research does not support the conclusion that improvement in these blood parameters is associated with a reduced risk of cirrhosis in the long term.

Tip: Probiotics can come with side effects, read more about those and whether they apply to you in our other article Probiotics Side Effects: Undesirable Things You Might Experience

Related postHow Should Probiotics Be Taken with Antibiotics? Gut Protection Insights

Can fatty liver disease affect your bowels? Conclusion

The liver has multiple functions that are vital for our body. If your liver is unhealthy it can affect your bowels, especially in the case of fatty liver disease.

It is necessary to ensure that the liver functions correctly to prevent possible fatty liver diseases or intestinal dysbiosis.

Preliminary research has shown the effectiveness of an omega-3-rich diet in improving metabolic syndrome and liver function.

Adopt and stick to a healthy lifestyle by:

  • limiting your consumption of alcoholic beverages,
  • promoting a healthy and balanced diet,
  • and, above all, practicing regular physical activity.
About Heather Campbell

As a nutritionist, my field of specialization is science-based nutritional advice but more importantly, it is my goal to share capturing and inspiring stories, examples and solutions which can help plus-size individuals overcome their specific difficulties. Read More