When it comes to NAFLD, obesity, and diabetes, physicians look signs of oxidative stress and inflammation. Often, the first place that they look is the digestive system.9
This makes sense. The liver receives about 70% of its blood supply from the intestine. Because of this, the liver is the first line of defense against food, environmental toxins, and disease-causing bugs.
When the gut becomes permeable, or “leaky,” a lot of foreign material can make its way deeper into the body, where it doesn’t belong.10 Oftentimes, the first stop is the liver.
One hallmark of leaky gut is the presence of bacterial endotoxin, which irritates and inflames the lining of the intestinal wall. In those who have an inflamed and irritated gut lining, we often see endotoxin and other traces of gut bacteria in the liver.11
Bacterial endotoxin, or lipopolysaccharide (LPS), is a component of the cell wall of some bacteria. Endotoxin is widely understood as a pro-inflammatory agent in the body. This means that wherever you find endotoxin, you will most likely find oxidative damage, inflammation, and disease.12, 13
Another hallmark of leaky gut is something called small intestine bacterial overgrowth (SIBO).
SIBO is exactly as it sounds. It is a situation where bacteria have grown to such proportions that they generate digestive discomfort like heartburn and, in some cases, have a hand in the development of more chronic forms of disease.
It turns out that small intestinal bacterial overgrowth occurs in a large percentage of people with chronic liver disease.14, 15, 16, 17
The Importance of Diet and Healthy Gut Bacteria
Currently, scientists are investigating which strains of bacteria do what. Once they determine which beneficial bugs are best suited for certain diseases, a probiotic drug can be developed.18
Until then, researchers are coming to the same conclusions over and over again: diet matters.
What we eat influences which bacteria populate the gut.
What we eat can also influence intestinal permeability. In fact, those with celiac disease have a notoriously permeable gut. They also are more likely to develop NAFLD.19
When we eat fermented foods and drink probiotic beverages, such as coconut water kefir, we receive a complete spectrum of good bacteria that have many health benefits. This includes helping to seal the lining of a leaky gut and combating oxidative stress.
As interest in our inner ecology grows in the medical field, researchers are finding that gut bacteria have huge therapeutic potential.
[+] Sources and References
1 E Vanni, et al. The gut-liver axis in nonalcoholic fatty liver disease: Another pathway to insulin resistance?. Hepatology. 2009; 49: 1790 – 1792. doi: 10.1002/hep.23036
2 M Lazo M, et al. Non-alcoholic fatty liver disease and mortality among US adults: prospective cohort study. BMJ. 2011; 343 (Nov 18): d6891. doi:10.1136/bmj.d6891
3 A Iacono, et al. Probiotics as an emerging therapeutic strategy to treat NAFLD: focus on molecular and biochemical mechanisms. The Journal of Nutritional Biochemistry. 2011 Aug; 22 (8): 699 – 711. doi:10.1016/j.jnutbio.2010.10.002
4 Backhed F, Ding H, Wang T, Hooper LV, Koh GY, Nagy A, et al. The gut microbiota as an environmental factor that regulates fat storage. Proc Natl Acad Sci U S A 2004; 101: 15718–15723.
5 Ley RE, Backhed F, Turnbaugh P, Lozupone CA, Knight RD, Gordon JI. Obesity alters gut microbial ecology. Proc Natl Acad Sci U S A 2005; 102: 11070–11075.
6 Turnbaugh PJ, Ley RE, Mahowald MA, Magrini V, Mardis ER, Gordon JI. An obesity-associated gut microbiome with increased capacity fro energy harvest. Nature 2006; 444: 1027–1031.
7 G Musso, et al. Gut microbiota as a regulator of energy homeostasis and ectopic fat deposition: mechanisms and implications for metabolic disorders. Lipidology. 2010 Feb; 21 (1): 76 – 83. doi: 10.1097/MOL.0b013e3283347ebb
8 ME Dumas, et al. Metabolic profiling reveals a contribution of gut microbiota to fatty liver phenotype in insulin-resistant mice. Proc Natl Acad Sci U S A. 2006 Aug 15;103(33):12511-6. Epub 2006 Aug 8. doi: 10.1073/pnas.0601056103
9 A. Abu-Shenab, et al. The role of the gut microbiota in nonalcoholic fatty liver disease. Nature Reviews Gastroenterology and Hepatology. 2010 Dec; 7, 691-701. doi:10.1038/nrgastro.2010.172
10 D Compare, et al. Gut–liver axis: The impact of gut microbiota on non alcoholic fatty liver disease. Nutrition, Metabolism and Cardiovascular Diseases. 2012 Jun; 22 (6): 471 – 476. doi: 10.1016/j.numecd.2012.02.007
11 DE Fouts, et al. Bacterial translocation and changes in the intestinal microbiome in mouse models of liver disease. J Hepatol. 2012 Jun;56(6):1283-92. Epub 2012 Feb 9.
12 E Albano, et al. Review article: role of oxidative stress in the progression of non-alcoholic steatosis. Alimentary Pharmacology & Therapeutics. 2005; 22: 71 – 73. doi: 10.1111/j.1365-2036.2005.02601.x
13 A Farhadi, et al. Susceptibility to gut leakiness: a possible mechanism for endotoxaemia in non-alcoholic steatohepatitis. Liver International, 2008; 28: 1026 – 1033. doi: 10.1111/j.1478-3231.2008.01723.x
14 L Miele, et al. Increased intestinal permeability and tight junction alterations in non-alcoholic fatty liver disease (NAFLD). Heptology. 2009. doi:10.1002/hep.22848.
15 AJ Wigg. The role of small intestinal bacterial overgrowth, intestinal permeability, endotoxemia, and tumour necrosis factor α in the pathogenesis of non-alcoholic steatohepatitis. Gut 2001; 48: 206–211.
16 Sajjad A, Mottershead M, Syn WK, Jones R, Smith S, Nwokolo CU. Ciprofloxacin suppresses bacterial overgrowth, increases fasting insulin but does not correct low acylated ghrelin concentration in non-alcoholic steatohepatitis. Aliment Pharmacol Ther 2005; 22: 291–299.
17 Sabaté JM, Jouët P, Harnois F, Mechler C, Msika S, Grossin M, et al. High prevalence of small intestinal bacterial overgrowth in patients with morbid obesity: a contributor to severe hepatic steatosis. Obes Surg 2008; 18: 371.
18 Y Sanz, et al. Probiotics as drugs against human gastrointestinal infections. Recent Pat Antiinfect Drug Discov. 2007 Jun;2(2):148-56.
19 L Abenavoli, et al. A pathogenetic link between non-alcoholic fatty liver disease and celiac disease. Endocrine. 2012. doi: 10.1007/s12020-012-9731-y