What Does Gut Bacteria Have To Do With Your Liver?
By Kathi Head, ND for Thorne Research
Fatty liver disease has reached epidemic proportions in the developed world, including the U.S. and Canada. In this condition, excess fat cells are stored in the liver, causing liver inflammation as well as potential scarring and damage. It can be caused by obesity, insulin resistance, high triglycerides, or other health-related causes. But, did you also know that the microbes that inhabit your gut can have a profound effect on the health of your liver?
It's well known that the human microbiome—the gut flora, plus all their metabolites—play a huge part in the health of your gut. But, it turns out that the microbiome can also affect the liver. When you have gut dysbiosis, too much of the wrong bacteria, it can cause inflammation in the gut.
Gut inflammation then leads to leaky gut, a condition which allows molecules that are larger than normal into the circulation system. This causes a chain reaction to occur that eventually leads to inflammation in the liver. This process is further exacerbated because there is a direct route from the GI tract to the liver, via the portal vein. The portal vein allows undesirable content in the gut to be deposited directly into the liver.
The key by-products of the gut bacteria that lead to a fatty liver are called lipopolysaccharides (LPS), which contribute to further inflammation and insulin resistance. In addition, sugar, in particular high-fructose corn syrup (HFCS), is one of the biggest culprits in the pathogenesis of fatty liver. Fructose contributes to fat accumulation in the liver by going directly to the liver, where it sets in motion the formation of fats in the form of triglycerides right there in the liver.
In addition, another way that fructose can contribute to a fatty liver is by altering the gut microbiome. The dysbiosis associated with HFCS intake results in loss of tight-junction proteins in the walls of the small intestine, which can lead to leaky gut and the translocation of endotoxins from the intestines into the bloodstream and liver. This sets up another adverse chain reaction that results in increased liver inflammation.
1. Probiotics—In animal studies of fatty liver, probiotics have been shown to preserve the tight-junction proteins in the small intestine, thus protecting the gut barrier that helps to decrease its leakiness. LPS levels in the bloodstream were also decreased. This resulted in livers that were less swollen, fatty, and inflamed.2 Another study found that feeding mice an obesogenic diet, with added Lactobacillus reuteri, prevented obesity and the development of a fatty liver as compared to mice given the same obesogenic diet without the probiotic.3
2. Prebiotics—In another animal model, a diet that included the prebiotic partially hydrolyzed guar gum resulted in healthy blood sugar levels and decreased fat accumulation in the liver.4
3. Mediterranean Diet—Numerous studies have shown that the Mediterranean diet, with its primary focus on vegetables, fruits, nuts, olive oil, and fish is beneficial for individuals with a fatty liver. For example, in one study 46 adults with fatty liver ate a Mediterranean diet for six months. Their liver fat scores and liver enzymes improved significantly.5 The Mediterranean diet supports a healthy gut flora because of its high fiber content and the presence of anti-inflammatory and antioxidant plant flavonoids.
In conclusion, studies have shown that bad gut flora can contribute to the development of digestive system inflammation, leaky gut, and fatty liver disease. But, with the right diet along with prebiotics and probiotics supplementation, your body can help combat the negative effects of bad bacteria. Start the New Year off right with these health choices that support your health from the inside out!
1. Lambertz J, Weiskirchen S, Landert S, Weiskirchen R. Fructose: Front Immunol 2017; 8:1159 doi: 10.3389/ fimmu.2017.01159.
2. Xue L, He J, Gao N, et al. Sci Rep 2017; 7: 45176. doi: 10.1038/srep45176.
3. Fak F, Backhed F. PLoS One 2012; 7(10): e46837. doi: 10.1371/journal.pone.0046837.
4. Naito Y, Ichikawa H, Akagiri S, et al. J Clin Biochem Nutr 2016; 58(1):23-33.
5. Gelli C, Tarocchi M, Abenavoli L, et al. World J Gastroenterol 2017; 23(17):3150-3162.
*These statements have not been evaluated by the FDA. These products are not intended to diagnose, treat, cure, or prevent any disease